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PAT202 WINTER > w4 management of acute and chronic illness diabetes > Flashcards

w4 management of acute and chronic illness diabetes Flashcards

1
Q

what are acute complications of diabetes mellitus?

A

-Hypoglycemia

-Counter-Regulatory Mechanisms
Somogyi effect
dawn phenomenon

-Diabetic ketoacidosis (DKA)

-Hyperosmolar hyperglycemic Nonketotic Syndrome (HHNKS)
also known as Hyperglycemic Hyperosmolar State (HHS)

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2
Q

what is hypoglycemia

A 
-Lowered plasma glucose level
	children and adults: less than 4 mmol/L (3.9 or less)
-Called insulin shock, insulin reaction
-Clinical manifestations
	tachycardia, palpitations, diaphoresis, tremors, pallor, and arousal anxiety
-Treatment
	oral or IV glucose
		D50W
	glucagon: prescribed for emergency use
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3
Q

what are symptoms of hypoglycemia? Neurogenic Adrenergic Symptoms (activation of the SNS)

A
  • tachycardia
  • palpitations
  • diaphoresis
  • tremors
  • pallor
  • arousal anxiety
  • hunger
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4
Q

what is hypoglycemia? Neuroglycopenic Symptoms

abrupt cessation of glucose delivery to brain

A
  • headache
  • dizziness
  • blurred vision
  • irritability
  • fatigue
  • poor judgment
  • confusion
  • seizures
  • coma
  • death
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5
Q

somogyi effect

A

-Hypoglycemia ~3:00am
too much intermediate-acting insulin given at dinner time followed by rebound hyperglycemia

-Hyperglycemia caused by secretion of counter-regulatory hormones (epinephrine, GH, corticosteroids)
stimulated by hypoglycemia → gluconeogenesis

-+++ carbohydrate intake may contribute to rebound hyperglycemia

-Treatment
decrease evening insulin level

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6
Q

what is dawn phenomenon?

A

-Early morning rise in BG without nocturnal hypoglycemia
different from Somogyi effect!
-Related to nocturnal growth hormone elevation
decreases metabolism of glucose by muscle and fat
-Treatment
alter timing and dose of insulin
increase dose of evening insulin

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7
Q

diabetic ketoacidosis (DKA)

A

-Absolute or relative deficiency of insulin and increase in counter-regulatory hormones
-Precipitating factors
-poor adherence to insulin treatment
-interruption of insulin admin
-infection
-trauma
-surgery
-MI
-Increased fat mobilization with release of fatty acids
leads to production of keto acids

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8
Q

what is happening in DKA?

A

-Most common in type 1 diabetes
-Less likely in type 2 diabetes
but can happen!

  • Extreme hyperglycemia, osmotic diuresis
  • Body metabolizes lipids to ketone bodies to create source of energy for cells
  • Ketone bodies reduce pH of blood causing metabolic acidosis
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9
Q

What is the pathophysiology of DKA ?

A

-Caused by increased levels of circulating ketones in absence of antilipolytic effect of insulin
-Because glucose is unable to enter cells, lipids are used as energy source and keto acids are produced as waste products
-High levels of keto acids lower pH of blood, causing diabetic ketoacidosis
drop in pH triggers buffering system associated with metabolic acidosis
-May progress to coma and possible death if untreated

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10
Q

What are signs and symptoms of DKA

A
  • ketonuria
  • polyuria
  • dehydration
  • thirst
  • Kussmaul respirations
  • acetone (fruity) breath odor
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11
Q

What are the treatments of DKA

A

insulin
-decrease BG levels
fluids
-replace lost fluid volume (osmotic diuresis d/t hyperglycemia)

electrolytes
-K+ most important electrolyte
can shift into and out of cells!!!

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12
Q

What is the pathophysiology of HHNKS

A

Factors
-insulin deficiency and increased levels of counter-regulatory hormones (glucagon, catecholamines, cortisol, growth hormone)
-increased gluconeogenesis and glycogenolysis
inadequate use of glucose by peripheral tissues, primarily muscle
-Proinflammatory mediators (TNF-α, IL-6, IL-1β) promote insulin resistance and release of counter-regulatory hormones
-contributes to insulin resistance and hyperglycemia
-Insulin levels sufficient to prevent excessive lipolysis but not to use glucose properly
-characterized by a lack of ketosis

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13
Q

What are the clinical manifestations of HHNKS

A

-glycosuria, polyuria, dehydration, neurologic changes
Lab findings
-BG often more than 33 mmol/L
-absent or low urine ketones

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14
Q

What are the treatments for HHNKS

A
  • insulin infusion combined with fluid replacement

- electrolyte replacement

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15
Q

What is Chronic Hyperglycaemia AKA Glucose Toxicity in type 1

A

Hyperglycemia more than 6 mmol/L:
-chronic hyperglycemia =glucose toxicity =harmful metabolic effects
-tight glycemic control is important!!!
-reverse or slow glucotoxic effects of chronic hyperglycemia
Type 1 diabetes:
-progressive autoimmune destruction of pancreatic beta cells
-occurs from absolute insulin deficiency and increase glucagon

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16
Q

What is Chronic Hyperglycaemia AKA Glucose Toxicity in type 2

A
  • pancreas usually continues to produce some insulin but insulin produced is
  • either insufficient for needs of body (beta cell exhaustion)
  • is poorly utilized by tissue (insulin resistance)
  • or both
  • pulse hepatic glucose production
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17
Q

How Does Recurrent or Persistent Hyperglycemia Cause Chronic Complications?

A

-With recurrent or persistent hyperglycemia, glucose becomes irreversibly bound to collagen and other proteins, blood vessel walls, interstitial tissue, and within cells causing damage

  • thickens basement membranes
  • increases permeability in small blood vessels and nerves
  • induces release of inflammatory cytokines and growth factors
  • stimulate cellular proliferation in glomeruli, smooth muscle of blood vessels, and collagen -synthesis with fibrosis
  • induces lipid oxidation, oxidative stress, and inflammation
  • inactivates NO with loss of vasodilation and diminished endothelial function
  • causes procoagulant changes with promotion of platelet adhesion and reduced fibrinolysis
  • promotion of beta-cell apoptosis and insulin resistance
18
Q

How does Hyperglycemia affect the Metabolic Pathways?

A

-Hyperglycemia induces overproduction of oxygen free radicals (oxidative stress)

  • Activation of several metabolic pathways
  • Inflammation
  • Associated with insulin resistance and dyslipidemia
  • Results in atherogenesis and damage to large and small vessels
19
Q

What are the Chronic Complications of Diabetes Mellitus ?

A 
-Microvascular disease
.damage to capillaries
.diabetic retinopathy
.diabetic nephropathy
.diabetic neuropathies
-Macrovascular disease
.damage to medium and larger arteries
.coronary artery disease
.MI
.cerebral vascular disease
.peripheral vascular disease

-Infection

20
Q

What are the Chronic Complications of Diabetes Mellitus ?

A 
-Microvascular disease
.damage to capillaries
.diabetic retinopathy
.diabetic nephropathy
.diabetic neuropathies
-Macrovascular disease
.damage to medium and larger arteries
.coronary artery disease
.MI
.cerebral vascular disease
.peripheral vascular disease

-Infection

21
Q

What are the characteristics of Microvascular Disease

A

-Damage to capillaries

-Characteristics
	hyperglycemia (must be present)
	hypoxia and ischemia
	thickening of capillary basement membrane
	endothelial cell hyperplasia
	thrombosis
	pericyte degeneration
22
Q

What is Diabetic Retinopathy ?

A

-Leading cause of blindness worldwide
-Develops more rapidly in type 2 diabetes
-Maculopathy
.progressive process that accompanies retinal capillary permeability, vessel occlusion, ischemia
-Macular edema
.fluid accumulation and retinal thickening

-Treatment
.laser treatment, vitrectomy, intravitreal steroids, antivascular endothelial growth factor, and renin-angiotensin system inhibitors

23
Q

What is the Screening For Retinopathy ?

A

Type 1 diabetes
every year starting 5 years after diagnosis in all individuals 15 years of age or older
Type 2 diabetes
-children, adolescents, and adults at time of diagnosis
-interval for follow-up assessment should be tailored to severity of retinopathy
-in those with no or minimal retinopathy, recommended interval is 1 to 2 years

24
Q

What is Diabetic Nephropathy ?

A

-Most common cause of end-stage kidney disease

-Progressive changes
.glomerular enlargement, glomerular basement membrane thickening

-Microalbuminuria
.first manifestation

-Treatment
.tight glucose control
.ACEIs or ARBs
.aggressive treatment of hypertension

25
Q

What is the Screening For Chronic Kidney Disease (CKD) ?

A

Type 1 diabetes
5 years after diagnosis and repeated yearly thereafter
Type 2 diabetes
start at diagnosis of diabetes and repeated yearly thereafter

26
Q

What is the Diabetic Nephropathy Pathophysiology ?

A

-Glomeruli injured by
.protein denaturation
.hyperglycemia with high renal blood flow (hyperfiltration)
.activation of RAAS
.production of angiotensin II (intraglomerular HTN exacerbated by systemic HTN)
-Progressive changes include
.glomerular enlargement
.glomerular basement membrane thickening
.proliferation of mesangial cells and matrix
-Later in the disease, this results in
.diffuse and nodular glomerulosclerosis
.loss of podocytes
.resistance to glomerular capillary blood flow
.decreased glomerular filtration rate (GFR)
-Alterations in glomerular membrane permeability
.albuminuria
-Tubular and interstitial fibrosis
.proximal tubule is particularly vulnerable

27
Q

What are the manifestations of Diabetic Nephropathy ?

A

-Before proteinuria
.clinical S&S of progressive glomerulosclerosis not likely
-Microalbuminuria is first manifestation
.develops within 5 to 10 years of disease
-Later
.hypoproteinemia, reduction in plasma oncotic pressure, fluid overload, anasarca (generalized body edema), and HTN may occur
-As GFR drops
.uremic signs, such as nausea, lethargy, acidosis, anemia, and uncontrolled hypertension, occur
-Macroalbuminuria
.strongly correlated with morbidity and mortality from cardiovascular disease, particularly in type 2 diabetes

28
Q

What are Diabetic Neuropathies?

A

-Most common complication of diabetes
-Sensory deficits generally precede motor involvement
-Peripheral neuropathy
.distal portions of neurons initially affected and eventually more severely affected
.axonal and Schwann cell degeneration
-Distal symmetrical polyneuropathy
.includes large and small nerve fibers
.small: neuropathic pain, loss of sensation
.large: sensory loss of proprioception

-Extremities involved first in a “stocking and glove” pattern

29
Q

What are MACROVASCULAR COMPLICATIONS ?

A
  • Coronary artery disease
  • MI
  • Cerebral vascular disease
  • Peripheral vascular disease
30
Q

What is Cardiovascular Disease?

A 
-Cause of death in up to 68% of people with diabetes
.accelerated atherosclerosis
.HTN
.increased risk for thrombus formation  
-Can result in
.CAD
.HF
.MI
-MIs often asymptomatic as a result of sensory and autonomic neuropathy
31
Q

Stroke and Diabetes

A

-Twice as common in those with diabetes
especially, type 2

-Risk factors
.HTN
.hyperglycemia
.hyperlipidemia
.thrombosis

-Survival rate for those with diabetes after massive stroke is often shorter than for someone without diabetes

-Treatment
.aggressive management of BP, hyperglycemia, lipidemia

32
Q

Peripheral Artery Disease (PAD)

A

-Incidence increases in those with diabetes (especially type 2)

-Risk factors
.age
.duration of diabetes
.glycemic control
.genetics

-Occlusions of small arteries/arterioles (especially below the knee) cause gangrenous changes of lower extremities
.lesions begin as ulcers
.progress to osteomyelitis or gangrene
.amputation

33
Q

Foot Care Checklist

A

EDUCATE
about proper foot care
EXAMINE
for structural, vascular, neuropathy problems at diagnosis then annually
DO
a 10 gram monofilament assessment
IDENTIFY
those at high risk of foot ulcers and educate, assess more frequently, consider footwear
REFER
persons with foot ulcers and other complications to those specialized in foot care

34
Q

Screening for Protective Sensation Using 10 gram Monofilament

A

How to Apply the monofilament:
Repeat this application twice at the same site, but alternate this with at least one ‘mock’ application in which no filament is applied (total three questions per site). Protective sensation is present at each site if the patient correctly answers two out of three applications. Incorrect answers – the patient is then considered to be Protective sensation is absent with two out of three at risk of ulceration.

35
Q

What are the infection risks of Diabetes

A

-Morbidity and mortality from infectious agents increase in those with diabetes

-Risk for infection increases because of
.impaired senses
.hypoxia
.rapid replication of pathogens from increased glucose
.decreased blood supply
.suppressed immune response
.delayed wound healing
36
Q

What are the ABCDES of Diabetes care?

A

A • A1C – optimal glycemic control (usually ≤7%)
glucose monitoring remains a cornerstone of diabetes management
allows people living with diabetes and their health-care providers to assess glycemic status and adverse effects, and to determine the effectiveness of glucose lowering therapies
B • BP – optimal blood pressure control (<130/80)
C • Cholesterol – LDL <2.0 mmol/L or >50% reduction
D • Drugs to protect the heart
A – ACEI or ARB │ S – Statin │ A – ASA if indicated│SGLT2i/GLP-1
E • Exercise / Healthy Eating
S • Screening for complications
S • Smoking cessation
S • Self-management, stress and other barriers

A • A1C – optimal glycemic control (usually ≤7%)
glucose monitoring remains a cornerstone of diabetes management
allows people living with diabetes and their health-care providers to assess glycemic status and adverse effects, and to determine the effectiveness of glucose lowering therapies
B • BP – optimal blood pressure control (<130/80)
C • Cholesterol – LDL <2.0 mmol/L or >50% reduction
D • Drugs to protect the heart
A – ACEI or ARB │ S – Statin │ A – ASA if indicated│SGLT2i/GLP-1
E • Exercise / Healthy Eating
S • Screening for complications
S • Smoking cessation
S • Self-management, stress and other barriers

37
Q

Key message

A

Optimal glycemic control is fundamental to the management of diabetes

Both fasting and postprandial plasma glucose levels correlate with the risk of complications

38
Q

What is A1C?

A

-indicates % of RBC hemoglobin that glucose is bound to
.process called glycosylation (glycosylated hemoglobin)
.assessed periodically to estimate overall glucose control over life of RBCs i.e. ~ 90-120 days

  • Higher levels of A1C = persistently elevated BG
  • Target A1C level of less than 7% is desirable to prevent complications

-Advantages over FPG include
.useful in determining glycemic control over time
.greater convenience as fasting not required
.fewer day to day alterations during periods of stress and illness

-Disadvantage
.does not provide information that can inform immediate/short-term decisions

39
Q

Physical Activity

A 
TRY
	to do a minimum of 150 minutes of moderate-to vigorous-intensity aerobic exercise per week
INCLUDE
	resistance exercise ≥ 2 times a week
SET
	physical activity goals and INVOLVE an interprofessionalteam
MINIMIZE
	uninterrupted sedentary time
40
Q

What is the Glycemic Index (GI) ?

A

Used to describe rise in BG levels after a person has consumed carbohydrate-containing food

Foods of low GI converted to sugar slower than white bread → steadily ↑BG
i.e. oat bran cereal, baked beans

Foods of high GI converted to sugar faster than white bread → cause sharp rise in BG
i.e. French fries, corn flakes, baked potato

Soluble fibre, fats, proteins slow gastric emptying
foods digested more slowly →↓ in glycemic response

41
Q

Type 2 Diabetes and Weight Loss

A
  • Nutritionally balanced, calorie-reduced diet should be followed to achieve and maintain a lower, healthier body weight
  • Weight loss results in improved insulin sensitivity and glucose tolerance, preserves beta-cell function, and has an inhibitory effect on progression to type 2 diabetes
42
Q

Alcohol, Insulin, and Oral Antihyperglycemics

A
  • Alcohol inhibits gluconeogenesis → hypoglycemia!
  • can occur up to 24 hours after, in those with type 1 diabetes
  • when taken with some oral antihyperglycemic drugs that increase insulin secretion → severe hypoglycemia
  • alcohol can also cause other serious adverse effects when used in conjunction with certain OHAs used to treat diabetes
  • risk of lactic acidosis in clients who use metformin
  • when alcohol is taken with sulfonylureas, some clients experience a serious disulfiram (Antabuse)-like reaction
  • flushing, angina, palpitations, vertigo, nausea
  • serious reactions, such as seizures and possibly death, also may occur

PAT202 WINTER (16 decks)

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