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NUE 325: Pathopharm I > Diabetes > Flashcards

Diabetes Flashcards

1
Q

diabetes

A

metabolic disorder characterized by hyperglycemia that results from insulin secretion, insulin action, or both
- associated with extensive long term damage when uncontrolled

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2
Q

carbohydrate

A

simple sugars and complex chemical units

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3
Q

where are carbs broken down

A

duodenum and proximal jejunum

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4
Q

normal health human glucose trends

A

blood glucose rises after you eat, then will lower back to baseline

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5
Q

diabetes

A
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6
Q

role of liver in glucose levels

A
  • extracts glucose
  • synthesizes glucose into glycogen for storage
  • glycogenolysis: break down of glycogen
    liver will inc glucose levels, which stimulates the pancreas to secrete insulin
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7
Q

what do peripheral tissues use for energy

A

glucose

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8
Q

role of the pancreas w glucose levels

A
  • exocrine function: secrete enzymes into the ducts of GI tract for breakdown
  • endocrine function: secrete insulin directly into the blood
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9
Q

islets of langerhans

A

islands of cells in pancreas that secrete glucagon and insulin
- alpha: secrete glucagon when low blood sugar
- beta: produce and secrete insulin which inc in blood sugar

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10
Q

glucagon

A

release by alpha cells when glucose levels are low
- stimulates glycogenolysis to begin (breakdown glycogen into glucose)

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11
Q

insulin

A

released from beta cells when glucose in blood is inc to promote intake of glucose into cells
- stimulates uptake, utilization, and storage of glu
- stimulates liver to store glu
- dec plasma conc of glu

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12
Q

hormones that lower blood glucose

A
  • insulin
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13
Q

hormones that increase blood glucose

A
  • glucagon
  • epi
  • glucocorticoids
  • growth hormones
    together balance glucose levels against insulin to prevent hypoglycemia
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14
Q

insulin and lipid metabolism

A
  • insulin promotes synthesis of fatty acids in the liver once the liver has been saturated w glycogen
  • insulin inhibits the breakdown on adipose tissue which can cause a buildup of TGs in fat cells
  • drives cells to use carbs instead of fat E
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15
Q

what happens when not enough insulin

A
  • cannot breakdown carbs
  • dec glucose
  • causes rapid glucose build up in blood –> hyperglycemia
  • cells can use alt sources of E like fatty acids
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16
Q

insulin deficiency: inc lipolysis

A

inc lipolysis (breakdown) and dec lipogenesis (formation)
- causes free FA in blood which is an alternate energy source, converted into cholesterol and phospholipids, and breaks down into acetyl-coA
- results in ketone bodies

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17
Q

ketone bodies

A

substances that are composed of acid breakdown byproducts

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18
Q

short term complications of impaired fat metabolism

A

increase serum ketones
- ketosis, measured by blood and urine levels of ketones
- ketosis can cause severe metabolic acidosis which can lead to coma

19
Q

long term complications of impaired fat metabolism

A
  • atherosclerosis bc his serum lipid levels
20
Q

insulin deficiency: protein metabolism

A

body unable to store protein effectively
- inc protein catabolism
- cessation of protein synthesis

21
Q

what can protein metabolism in insulin deficiency result in

A
  • inc protein breakdown means more aa in blood
  • inc use of aa as energy storage
  • protein catabolism results in muscle wasting, multiple organ dysfunction, aminoacidemia, inc BUN
22
Q

insulin deficit: fluid and electrolytes

A

inc serum glucose levels –> increased plasma oncotic pressure –> fluid shifts into intravascular compartment –> intracellular dehydration
glucose isnt being taken but, blood becomes super conc w glucose, water moves out of cells dehydrating them and in to vascular space

23
Q

glycosuria

A

excretion of sugar in the urine
- occur when hyperglycemia inc beyond what kidneys can reabsorb
- + urine dipstick
- inc acetones in urine

24
Q

polyphagia

A

increased hunger
- due to catabolism (breakdown) of fat and protein, cell starvation

25
Q

polydipsia

A

excessive thirst
- due to inc serum osmolality

26
Q

polyuria

A

excessive urination
- due to osmotic diuresis

27
Q

DM

A

group of metabolic disorders characterized by hyperglycemia resulting from absolute or relative insulin deficiency

28
Q

type 1 D

A

complete lack of endogenous insulin
- most common pediatric disease –> usually around 12 yr old
- can be idiopathic
- usually an autoimmune process –> genetic predisposition and env factors
t cell mediated disease destroys beta cells

29
Q

clinical manifestations of type 1 D

A

long preclinical period of symptoms until the insulin production is almost to none
- results in hyperglycemia producing symptoms
- symptoms: 3 p’s, weight loss, fatigue, recurrent infections, prolonged wound healing, visual changes, parathesias, cardio symptoms

30
Q

type 2 d

A

insulin resistance and some dec insulin production
- genetic - environmental aspect usually responsible
- risk factors: age, obesity, HTN, physical inactivity, family history
- suboptimal response of insulin resistant tissue

31
Q

types of risk factors for type 2 D

A

modifiable: physical inactivity, high body fat, high blood pressure, high cholesterol
non modifiable: history of gestational, race/ethnicity, over 45 yo, family history

32
Q

type 2 clinical manifestation

A

usually just vague/non specific manifestations of hyperglycemia like fatigue, recurrent infections, visual changes, prolonged wound healing
- usually diagnosis by dr testing bc of risk factors

33
Q

complications associated w type 2

A
  • impaired insulin secretion
  • peripheral insulin resistance
  • increased hepatic glucose production
  • altered production of hormones and cytokines by adipose tissue
34
Q

acute complications of d

A

DKA: type 1, insulin deficiency so hyperglycemia, acidosis, ketonuria
HHNS: type 2, less profound insulin deficiency but more significant fluid deficiency (fluid shifting)

35
Q

hypoglycemia

A

rapid onset, blood sugar below 55-60
- usually related to medications
- symptoms: pallor, sweating, tachycardia, palpations, hunger, restlessness, anxiety, tremors, convulsions, coma

36
Q

problems w poorly controlled diabetes

A
  • insulin resistance/deficit, chronic hyperglycemia, accumulation of advanced glycation end products, activation of metabolic pathways that cause damage
37
Q

micro vascular

A

damages to capillaries
- retinopathies, nephropathies, neuropathies
- frequency and severity of lesions are proportional to disease
- accompanied by hypoxia and ischemia
- associated w capillary membrane thickening (microangiopathy: small vessel disease)

38
Q

macrovascular

A

damage to large vessels
- coronary artery, peripheral vessels, cerebral vascular

39
Q

diabetic neuropathy

A

loss of pain, temperature, and vibration sensations that can lead to ulcers, infection, possible amputation
- most common complication
- cause ischemia and demyelination, delaying conduction

40
Q

diabetic retinopathy

A

results from relative hypoxemia, damage to retinal blood vessels, red blood cell aggregation and HTN
–> small vessels become occluded causing infarction
- leading cause of blindness world wide

41
Q

diabetic nephropathy

A

glomerular basement membrane thickens and become sclerosed –> nonfunctional
- diabetes cause chronic kidney disease and end stage kidney disease

42
Q

macrovascular complications

A

atherosclerosis: thickening, hardening of large arteries
- coronary artery disease, peripheral vascular disease, stroke, inc risk of infection
- thought to be result of oxidative stress, endothelial dysfunction, alterations in mineral metabolism, inc cytokine production

43
Q

diabetes and infection

A
  • diminished warning sign bc peripheral and retinal neuropathies
  • tissue hypoxia when skin becomes impaired and health cells cant get there to heal
  • rapid proliferation of pathogens bc of excess glucose feeding them
  • dec WBC

NUE 325: Pathopharm I (23 decks)

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