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NUR 325 - Intro to Pathopharm > WK 3 Diabetes Patho > Flashcards

WK 3 Diabetes Patho Flashcards

1
Q

Diabetes

A

metabolic disorder characterized by HYPERGLYCEMIA that results from defects in insulin secretion, insulin action, or both
- extensive long-term damage when uncontrolled

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2
Q

Carbohydrates (CHO)

A

simple sugars and complex chemical units
- are broken down in the duodenum and proximal jejunum
- blood glucose levels temporarily rise then lower back to baseline

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3
Q

Liver and glucose

A

regulating glucose depends on the liver
- extracts glucose from blood
- synthesizes it into glycogen (energy storage)
- glycogenolysis (breakdown glycogen)

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4
Q

Peripheral tissue (muscles and fat cells)

A

extract the glucose for their energy need

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5
Q

Pancreas

A

in connection with the liver, controls body’s fuel supply
- 2 major functions occur

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6
Q

Exocrine pancreas

A

pancreatic cells secrete directly into ducts (not bloodstream)

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7
Q

Endocrine pancrease

A

secrete insulin directly into bloodstream
our focus for diabetes

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8
Q

Islet of langerhans

A

pancreatic islets are small islands of cells within the pancreas that make up the endocrine function

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9
Q

Alpha cells

A

secrete glucagon in response to low blood sugar

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10
Q

Glucagon

A

stimulates the liver to release stored glucose into the blood

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11
Q

Beta cells

A

produce insulin, which lowers glucose levels by stimulating the movement of glucose into body tissues

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12
Q

Balancing act of hormones

A

insulin LOWERS blood glucose levels
several hormones RAISE blood glucose levels
- glucagon (islet of langerhans)
- epinephrine (adrenal medulla)
- glucocorticoids (adrenal cortex)
- growth hormones (anterior pituitary)

together these hormones create a counter-regulatory mechanism that prevents hypoglycemia under effect of insulin

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13
Q

Insulin

A

a hormone secreted by the pancreas (beta cells specifically) that stimulates:
- uptake, utilization, and storage of glucose
- the liver to store glucose (as glycogen)
BECAUSE OF ABOVE, insulin decreases plasma concentration of glucose

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14
Q

Insulin makes the glucose in your blood go….

A

DOWN

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15
Q

Insulin + lipid metabolism

A

insulin promotes synthesis of fatty acids in the liver -> this occurs once the liver has been saturated with glycogen

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16
Q

Insulin inhibits…

A

the breakdown of fat in adipose tissue, which can cause a buildup of triglycerides in fat cells

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17
Q

Lipid metabolism overall

A

insulin has a fat-sparing effect, and drives cells to use carbohydrates instead of fat for energy

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18
Q

When you don’t have enough insulin

A
  • cannot break down carbohydrates efficiently
  • decreased glucose (by-product of carbohydrate break down) use by cells
  • then rapid build of glucose in blood = HYPERGLYCEMIA
  • cells have to use alternate stores of energy = fatty acids
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19
Q

Insulin deficiency

A

impaired fat metabolism also occurs
- increased lipolysis (fat breakdown)
- decreased lipogenesis (formation of fat)
this causes FFAs

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20
Q

Free Fatty Acids (FFA)

A

in your blood
- FFA are an alternate energy source for tissues
- excess FFA is converted to cholesterol and phospholipids
- FFA breaks down to acetyl-CoA (used by liver) into ketone bodies

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21
Q

Ketone bodies

A

substance that are composed of these acid breakdown products

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22
Q

Short term complications of impaired fat metabolism

A
  • increased serum ketones = ketosis
  • measured by blood and urine levels of ketones
  • ketosis can cause severe metabolic acidosis -> coma
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23
Q

Long term complications of impaired fat metabolism

A

atherosclerosis because of high serum lipid levels

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24
Q

Insulin deficiency and protein metabolism

A
  • body is unable to store protein effectively
  • increased protein catabolism
  • cessation of protein synthesis
25
Protein metabolism causes...
- increased protein breakdown -> more amino acids in circulation - increased use of amino acids as alternative energy source - protein catabolism = muscle wasting
26
Advanced glycation end products
breakdown protein = more amino acids fat breakdown = FFA and ketone bodies
27
Protein catabolism
clinical picture - muscle wasting - multiple organ dysfunction - aminoacidemia - increased urea nitrogen (BUN) *** more typical in type 1 diabetic
28
Insulin deficit and fluid/electrolytes
- increased serum glucose levels -> increased plasma oncotic pressure -> fluid shifts into intravascular compartment -> intracellular dehydration -> osmotic diuresis
29
Insulin deficit and glycosuria
excretion of sugar in the urine - occurs when hyperglycemia increases beyond what the kidneys can reabsorb - positive urine dipstick - increased acetones in urine
30
Polyphagia
increased hunger - d/t catabolism of fat and protein and cellular starvation
31
Polydipsia
excessive thirst - d/t increased serum osmolarity
32
Polyuria
excessive urination - d/t osmotic diuresis - excreting water - loss of electrolytes - K, Na, Cl, others
33
Diabetes mellitus
group of metabolic disorders that are characterized by hyperglycemia, resulting from absolute or relative insulin deficiency 3 types: - type 1, type 2, gestational diabetes, other rare ones
34
Type 1 diabetes
most common pediatric chronic disease - usually diagnosed around 12yrs of age - can be idiopathic - much less common - usually an autoimmune process complete lack of endogenous insulin
35
T1DM autoimmune process
- genetic predisposition and environmental factors - slowly progressive disease - t-cell mediated disease that destroys beta cells
36
T1DM clinical manifestations
- dx around 11-13, can have adult onset - long preclinical period of symptoms until the production of insulin goes to almost none - results in hyperglycemia and produces symptoms - same diagnostic criteria as type 2
37
T1DM symptoms
- 3 ps - weight loss - fatigue - recurrent infections - prolonged wound healing - general pruritus - visual changes - paresthesias - cardiovascular symptoms
38
T2DM
genetic-environmental aspect usually responsible risk factors - age - obesity - HTN - physical inactivity - family hx - age over 45 years - race/ethnicity - hx of gestational diabetes
39
T2DM and insulin
INSULIN RESISTANCE and some decreased insulin secretion - suboptimal response of insulin-sensitive tissues (basically see it and they decided they don't need it because there is so much insulin all the time, insulin receptors on the cell become tired so they don't allow glucose into the cell, glucose stays in the blood) (beta cells can become tired and decreases insulin production)
40
T2DM clinical manifestations
- symptoms not as evident in type 2 - don't see the 3 ps as much - usually just vague s/s of hyperglycemia - fatigue, recurrent infections - visual changes, prolonged wound healing - doctors usually test for those at high risk
41
Metabolic complications with T2DM
- impaired insulin secretion -> beta cells exhaustion due to overuse - peripheral insulin resistance -> increased visceral fat - increased hepatic glucose production -> impaired suppression of gluconeogenesis within the liver - altered production of hormones and cytokines by adipose tissue
42
acute complications of diabetes
diabetic ketoacidosis (DKA) hyperosmolar hyperglycemic syndrome (HHNS)
43
Diabetic ketoacidosis
- more common in T1DM - serious complication related to insulin deficiency - characterized by hyperglycemia, acidosis, and ketonuria
44
Hyperosmolar hyperglycemic syndrome (HHNS)
- type 2 complication - extremely high hyperglycemia and osmolarity, normal pH - less profound insulin deficiency than DKA but more significant fluid deficiency
45
Hypoglycemia
happens in both types of diabetes rapid onset blood sugar less than 55-60 usually related to medications
46
Hypoglycemia symptoms
- pallor - sweating - tachycardia - palpitations - hunger - restlessness - anxiety - tremors - convulsion - coma
47
Chronic complications of diabetes
typically associated with poorly controlled diabetes - insulin resistance/deficit, chronic hyperglycemia, accumulation of advanced glycation end products (amino acids, ketone bodies, FFA), activation of metabolic pathways that cause tissues damage
48
Microvascular damage
damage to capillaries, retinopathies, nephropathies, and neuropathies
49
Macrovascular damage
damage to large vessels, coronary artery, peripheral vascular and cerebral vascular
50
Microvascular disease
frequency and severity of lesions appear to be proportional to duration of the disease - hypoxia and ischemia accompany microvascular disease usually in the eyes, kidneys, and nerves - associated with capillary membrane thickening
51
Microangiopathy
small vessel disease, capillary membrane thickening
52
Diabetic neuropathy
most common complication of diabetes - related to both metabolic and vascular factors associated with chronic hyperglycemia = cause ischemia and demyelination which causes neural changes and delayed conduction
53
Diabetic neuropathy s/s
- loss of pain, temperature, and vibration sensations - can lead to ulcers, infection, and result in amputation
54
Diabetic retinopathy
leading cause of blindness worldwide - results from relative hypoxemia, damage to retinal blood vessels, red blood cell aggregation and hypertension - small vessels become occluded, causes infarction
55
Diabetic nephropathy
- diabetes more common cause of chronic kidney disease and end stage kidney disease - glomerular basement membrane thickens and becomes sclerosed = thickened and hard, nonfunctional
56
Macrovascular complications
more common in type 2 diabetics - atherosclerosis = thicken, hard LARGE ARTERIES - CAD, PVD, CVA, increased risk of infection
57
Diabetes + infection
deadly combo - diminished warning signs = r/t peripheral and retinal neuropathies - tissue hypoxia = when skin becomes impaired, healthy cells cannot get there to heal it - rapid proliferation of pathogens - fungal/yeast/UTI/gangrene
58
rapid proliferation of pathogens
r/t excess serum glucose, which bacteria feeds on and decreased circulation of good WBCs (become abnormal and less effective)

NUR 325 - Intro to Pathopharm (22 decks)

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