Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

NURS 2514 > Week 2 - Diabetes > Flashcards

Week 2 - Diabetes Flashcards

1
Q

what is glycogen

A
  • major form of stored glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

where is glycogen primarily found

A
  • liver & muscle cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is glycogenolysis

A
  • the breakdown of glycogen to glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is gluconeogenesis

A
  • process of producing glucose from non-carbohydrate sources
    ex. proteins & fats
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is euglycemia? what is the range?

A
  • normal blood glucose

- 4-7 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is glycolysis

A
  • the breakdown of glucose into pyruvate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the role of insulin in regulating BG

A
  • released when BG is elevated

- brings BG back down to normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the counterregulatory hormones? what do they do & list them (4)

A
  • hormones that oppose insulin –> they elevate BG
    1. glucagon
    2. epi
    3. cortisol
    4. GH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is diabetes mellitus? what does it involve?

A
  • disorder of the endocrine pancreas

- involves a deficiency in insulin function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are 2 types of insulin dysfunction that occurs with DM

A
  1. decreased secretion
  2. tissue insensitivity (where they do not respond to insulin)
    - or both
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

DM is characterized by the presence of ______

A
  • hyperglycemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

in addition to hyperglycemia, diabetes can result in…. (3 things)

A
  1. increased catabolism of proteins & lipids
  2. acute emergencies
  3. chronic complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the endocrine pancreas cells called?

A

islets of langerhans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the 2 types of islets of langerhans

A
  • alpha & beta cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the function of alpha cells

A
  • secrete glucagon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the function of beta cells

A
  • secrete insulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what type of hormone is insulin? how does that impact the pharmacologic administration of it?

A
  • it is a protein hormone

= cannot be given orally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

insulin is manufactured exclusively by the _____

A
  • islet beta cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what happens to insulin once it is synthesized?

A
  • stored in vesicles & is secreted by exocytosis when needed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

insulin is a ____(anabolic or catabolic) hormone?

A
  • anabolic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the primary stimukus for insulin secretion

A
  • high blood glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

describe how high BG stimulates insulin secretion

A
  • glucose enters B cells & is converted into ATP thru glycolysis
  • increased cellular ATP closes ATP sensitive K+ channels (remember, K+ flows out) = membrane potential becomes more positive
  • this opens voltage-gated Ca++ channels which triggers release of insulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what else is insulin secretion stimulated by?

A
  • amino acids

- acetylcholine (PSNS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is insulin secretion inhibited by?

A
  • alpha-adrenergic stimulation (SNS)

- beta blockade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

insulin secretion is matched to _____ & ______

A
  • dietary intake & metabolic rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

describe the effects of glucagon: what stimulates the release? what happens in the body?

A
  • low blood sugar = promotes glucagon release
  • glucagon acts on the liver to promote glycogen breakdown into glucose
    = raised blood sugar
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

describe the effects of insulin: what stimulates the release? what happens in the body?

A
  • high BG = insulin release
  • this stimulates (1) glucose uptake from the blood into cells and (2) glycogen formation to be stored for later
    = decreased BG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

insulin also promotes the uptake of… (3)

A
  1. amino acids for protein synthesis
  2. fatty acids for storage of triglycerides
  3. uptake of K+ ions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

how many types of diabetes are ther?

A

4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is type 1 diabetes? what causes it?

A
  • autoimmune disease

- caused by a T-cell & antibody mediated immune assult on beta cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

how long does the attack on beta cells last during type 1 diabetes? what effect does this have on insulin?

A
  • typically does not stop until all beta cella are irreversibly lost
    = insulin secretion virtually nonexistent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

when do we start to see symptoms acutely in type 1 diabetes

A
  • when more than 70% of beta cell are eliminated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

describe treatment for patients with type 1 diabetes

A
  • life-long exogenous insulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is the typical age of onset for type 1 DM

A
  • usually under age of 30
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what are 2 other names for type 1 diabetes?

A
  • insulin-dependent diabetics
  • juvenille diabetes
    (but these arent rlly used anymore)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

describe what patients with type 1 diabetes typically look like?

A
  • nonobese

- with muscle wasting –> thin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is the most common type of diabetes

A
  • type 2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is the cause of type 2 diabetes? why is this thought to be the cause?

A
  • unknown
  • thought to be a combo of genetic & lifestyle factors
  • 80% of patients are obese (particular abdominal obesity) and 80% have family history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what are the 4 things that occur in the body with type 2 DM

A
  1. periphal insulin resistance which leads to decreased insulin-stimulated glucose uptake at the tissues
  2. hepatic glucose output is increased
  3. pancreas icreases its insulin secretion (to compensate for insulin resistance)
  4. altered carb absorption in the gut
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

describe the effect of type 2 DM on the liver

A
  • hepatic glucose output is increased = liver is constantly exporting glucose without any response to insulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

describe the changes seen in the pancreas during type 2 DM to compensate for insulin resistance; what does this cause?

A
  • increases its secretion of insulin
  • causes hyperinsulinemia in early stages
  • over time, it becomes exhausted which causes defective insulin secretion & diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is the age of onset for type 2 DM

A
  • typically adult
  • becoming common in adolescence
  • bc of the gradual onset, many cases go undiagnosed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

describe treatment for patients with type 2 DM

A
  • many do not require insulin treatment bc some residual insulin function remains
  • main is diet & exercise changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what is type 3 diabetes

A
  • miscellaneous category which represents many causes of primary or secondary diabetes
    (note: i did not list all the examples bc there is way too many, so see notes for that)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what is type 4 diabetes?

A
  • gestational diabetes

- occurs during the 3 trimester but resolves after parturition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

describe the risk of type 4 diabetes and how it changes with pregnancies

A
  • occurs in 5-10% of pregnant women

- risk increases with subsequent pregnancies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what is the cause of type 4 diabetes

A
  • attributed to increased levels of hormones with counterregulatory hormone effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

describe the risk of type 2 diabetes for a pt with type 4

A
  • type 4s have an increased risk of developing type 2 in future, especially obese women
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

list 2 consequences of type 4 diabetes

A
  • increased birth weight

- adverse maternal & fetal outcomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what is a key feature of diabetes

A
  • fasting & postprandial hyperglycemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what is the difference between fasting & postprandial BG levels

A
  • fasting = measures BG after a 8 h or more fast

- postprandial = measures BG after eating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

the degree of hyperglycemia & other metabolic abnormalities depend on….

A
  • the degree of insulin deficit
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

in addition to insulin deficiency, type 1 and type 2 diabetics also have….

A
  • elevated glucagon levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what is the glucose tolerance test?

A
  • helpful clinical tool to evaluate fasting & postprandial hyperglycemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

describe how the glucose tolerance test works

A
  • the pt fasts overnight & then we take their fasting BG
  • the pt then consumes a 75g glucose load
  • blood is then tested every 1/2 hour for 2-3 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what values indicate a positive glucose tolerance test

A
  • when the fasting BG is greater then 7 mmol OR

- if the postprandial BG exceeds 11.1 during the 2 hr followup

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what does pre-diabetes mean

A
  • term used when BG is elevated but still under the criteria
    ex. 10.9
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

describe the relation between glucose & proteins when BG is elevated

A
  • when BG is elevated, glucose non-enzymatically binds to proteins = glycosylation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what is glycosylated hemoglobin

A
  • HbA1C

- hemoglobin that is binded to glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

why do we measure the amount of glycosylated hgb?

A
  • way to determine if BG has been elevated any tme over the previous 90-120 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what value indicates normal vs diabetes in a glycosylated hgb test?

A
  • <5.5% = normal

- >6.5% = diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what effect does insulin deficiency have on VLDL and LDLs

A
  • elevated blood triglycerides & lipoproteins (VLDL & LDL)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what are the 4 main manifestations of type 1 diabetes

A
  1. glucosuria
  2. polyuria
  3. polydipsia
  4. polyphagia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what is glucosuria

A
  • glucose in the urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what is polyuria

A
  • enhanced production of urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what is polydipsia

A
  • excessive thirst
67
Q

what is polyphagia

A
  • excessive hunger
68
Q

can glucose pass thru the glomerular cap?

A
  • yes, it is small enough to pass thru the glomerular capillaries & enter into the tubule filtrate
69
Q

describe the reabsorption of glucose under normal conditions

A
  • normally, all of the filtered glucose is reabsorbed back into the blood by the sodium-dependent glucose transporter (SGLT) = none in the urine
70
Q

how does the reabsorption of glucose effect the reabsorption of water under normal conditions

A
  • as osmotically active molecules (Na and glucose) are removed from the filtrate, water is passively reabsorbed via osmosis
71
Q

explain why we get glucosuria with diabetes

A
  • with hyperglycemia, the amount of filtered glucose is greater than the tubules capacity to reabsorb (not enough SGLT)
    = some glucose remains in the filtrate & is excreted in the urine
72
Q

explain why we get polyuria with diabetes

A
  • due to glycosuria, there is a higher conc of glucose than normal in the filtrate
  • glucose is an osmotic molecule –> it attracts water to itself
    = impairs the osmosis of water where water less water is reabsorbed & causes osmotic diuresis
73
Q

explain why we get polydipsia with diabetes

A
  • due to polyuria, we are losing more water in the urine = dehydration = stimulated thirst response in the hypothalamuc
74
Q

explain why we get polyphagia with diabetes

A
  • significant calories are lost in the urine & appetite center in the hypothalamuc is activated
75
Q

what is DKA

A
  • acute diabetic emergency

- diabetic ketoacidosis

76
Q

what occurs in DKA

A
  • absence of insulin –> uncontrolled lipolysis & ketogenesis
  • this results in the formation of keto acids which enter the blood, accumulate, and causes metabolic acidosis
77
Q

who does DKA commonly occur in? what else might cause it?

A
  • common in type 1 diabetes

- or can occur with missed insulin dosage

78
Q

why is DKA more rare in type 2 diabetes

A
  • bc there is still some residual insulin function which inhibits profound lipolysis & ketogensis
79
Q

what is ketogenesis

A
  • the production of keto acids
80
Q

what might cause DKA in type 2s (3)

A
  • infection, trauma, and stress which can increase the body’s insulin demand
81
Q

what can happen if DKA is left untreated

A
  • coma & death
82
Q

what are the 3 major manifestations of DKA

A
  1. severe hyperglycemia
  2. metabolic acidosis
  3. rapid respirations & fruity breath
83
Q

what does severe hyperglycemia during DKA cause? (2)

A
  • profound diuresis (excessive amt of urine)

- loss of electrolytes (K+) in the urine

84
Q

what is metabolic acidosis

A
  • low pH due to low bicarb
85
Q

how does DKA cause metabolic acidosis?

A
  • uncontrolled ketogensis results in the production of keto acids
  • the keto acids react with bicarb to result in decreased bicarb
  • the keto acids also accumulate which contributes to low pH
86
Q

what does dehydration from polyuria & vomiting cause during metabolic acidosis due to DKA? (2)

A
  • hypovolemia

- lactic acidosis

87
Q

what causes rapid respirations during DKA

A
  • to compensate for the metabolic acidosis, the patient will have rapid, deep repirations to try & decrease CO2
88
Q

what are the rapid, deep respirations during DKA called?

A
  • Kussmaul
89
Q

what causes the fruity breath during DKA

A
  • ketones are spontaneously converted to acetone in the blood
  • the acetone vaporizes in the alveoli & gives the breath a fruity odor
90
Q

describe treatment for DKA

A
  • IV insulin therapy (since cause is absent insulin)
  • fluid management (bc often dehydrated)
  • K+ supplement
91
Q

why is a K+ supplement also required for treatment of DKA

A
  • insulin treatment will increase the cellular uptake
  • K+ is lost in the urine & vomit
  • is diluted with the fluid treatment
92
Q

hypoglycemia is a complication of… (2)

A
  • insulin therapy

- sulfonylureas

93
Q

list 4 causes of hypoglycemia

A
  • when the drug is over-administered
  • with exercise
  • with fasting or a missed meal
  • with excessive alcohol consumption
94
Q

hypoglycemia is sometimes referred to as…

A
  • insulin shock

not used much nowadays

95
Q

manifestations of hypoglycemia are caused by…

A
  • increased SNS stimulation (early signs)

- decreased CNS function (late signs)

96
Q

why does SNS stimulation occur during hypoglycemia

A
  • to try and raise the BG –> epi and norepi are released & are counter regulatory hormones for insulin
97
Q

what SNS effects are seen during hypoglycemia (7)

A
  • sweating
  • tachycardia
  • tremor
  • anxiety
  • hunger
  • palpitations
  • nausea
98
Q

at what BG level do we see SNS stimulation symptoms

A
  • below 3.5
99
Q

what causes CNS depression in hypoglycemia

A
  • bc the brain needs a constant supply og glucose
100
Q

what CNS effects are seen during hypoglycemia

A
  • confusion
  • irritability
  • headaches
  • loss of coordination
  • convulsion
  • coma
101
Q

at what BG level do we see CNS depression in hypoglycemia

A
  • below 2.5 mmol/L
102
Q

describe treatment for hypoglycemia

A
  • oral or IV glucose

- IV glucagon

103
Q

what can cause a reduced SNS response in hypoglycemia (2)? what are the consequences of this?

A
  • repeated bouts of hypoglycemia or beta-blocker can reduce the SNS response
    = become desensitized & get no warning signs
104
Q

what are the 3acute diabetic emergencies

A
  1. diabetic ketoacidosis
  2. hypoglycemia
  3. hyperosmolar coma
105
Q

what causes a hyperosmolar coma

A
  • as BG increases, we lose glucose & water in the urine and we become profoundly dehydrated
  • this dehydration & hyperglycemia causes hyperosmolarity (more solute than water)
  • this dehydration sucks water out of cells thru osmosis which is typically fine, except for in the brain
  • the dehydration causes cellular dehydration of CNS neurons which will impair cognitive function
106
Q

why is HHNC so dangerous?

A
  • since there is no ketoacidosis, there is no warning signs

= can creep up on them

107
Q

describe hyperosmolar coma in type 1 vs 2 diabetics

A
  • hyperosmolar comas occur type 1 diabetics due to DKA

- in type 2s severe coma can occur in the absence of ketosis

108
Q

what is a hyperosmolar hyperglycemic state (HHS)? what can it progress to?

A
  • a hyperosmolar hyperglycemic state is when someone has super high BG & is very dehydrated, causing hyperosmolarity and beginning to lose consciousness
  • can progress to a hyperosmolar hyperglycemic nonketotic coma (HHNC)
109
Q

who does a HNNC occur more commonly in

A
  • the elderly type 2 patient
110
Q

why dont type 2 diabetics get DKA

A
  • residual insulin function prevent ketoacidosis
111
Q

what is HHNC often precipitated by/contributing factors? (4)

A
  • inadequate fluid intake during another illness
  • infection
  • HF
  • MI
112
Q

why do the contributing factors often precipiate HHNC?

A
  • these increase CRH release & can compromise bp
  • the low bp can cause decreased GFR which means less glucose is lost in the urine, resulting in an even higher osmolarity
113
Q

what does the absence of ketoacidosis with HHNC result in?

A
  • patients are asymptomatic much longer = delayed care
114
Q

how high can BG be with HHNC

A
  • as high as 45-100 mmol
115
Q

describe the treatment for HHNC

A
  • same as DKA
116
Q

describe the mortality rate of HHNC compared to DKA

A
  • is 10x higher bc patients are often older & have srious complicating illnesses
117
Q

list 4 chronic complications of diabetes

A
  1. microvascular disease (microangiopathy)
  2. macrovascular disease (macroangiopathy)
  3. neuropathy
  4. infections & foot ulcers
118
Q

what are 2 kinds of microangiopathy

A
  1. retinopathy

2. nephropathy

119
Q

what are 3 kinds of macroangiopathy

A
  1. CAD
  2. cerebral artery disease
  3. peripheral artery disease
120
Q

what are 2 types of neuropathy

A
  1. peripheral neuropathy

2. autonomic neuropathy

121
Q

what is believed to reduce the incidence of chronic complications of diabetes?

A
  • proper glycemic control

- especially for retinopathy, nephropathy, and neuropathy

122
Q

what is microangiopathy

A
  • disease of small vessels

ex. capillaries

123
Q

what causes microangiopathy

A
  • believed to be directly related to hyperglycemia
124
Q

describe what occurs during microangiopathy

A
  • basement membranes of the capillaries thicken

- also causes increased collagen (makes it stiff) and decrease proteoglycan (makes it spongy)

125
Q

what is AGE? how are they formed

A

Advanced Glycosylation End-products

- with prolonged hyperglycemia, glucose irreversibly binds to proteins to create them

126
Q

describe how AGEs contribute to microangiopathy (4)

A

cause:

  • accumulation of basement membrane proteins
  • capture LDL
  • release inflammatory cytokines
  • can predispose to microaneuryms
127
Q

what is the leading cause of adult-onset blindness?

A
  • diabetes
128
Q

diabetic retinopathy ocurrs in __ stages; what are they

A
  1. nonproliferative

2. proliferative

129
Q

describe what occurs during the nonproliferative stage of retinopathy

A
  • microaneurysms occur in the retinal blood vessels due to microangiopathy & loss of pericytes
  • aneurysms become permeable or rupture = retinal exudate formation & hemorrhage = cells beyond the rupture do not get any blood
130
Q

what are the consequences of the nonproliferative stage of retinopathy

A
  • retinal ischemia & infarction due to lack of blood flow

- visual impairment such as blind spots due to healing with scar tissue & leakage of fluid

131
Q

describe what occurs during the proliferative stage of retinopathy

A
  • retinal ischemia stimulates angiogenesis within the retina
  • infarction of the retina causes fibrous scar tissue to replace necrotic neural tissue
  • as fibrous tissue accumulates, it pulls back the retina & creates tension
132
Q

what does proliferative retinopathy result in

A
  1. the tension on the retina can cause retinal detachment

2. blindness

133
Q

which type of diabetes dooes proliferative retinopathy occur more frequently in?

A

type 1 diabetes

134
Q

diabetes is the leading cause of end-stage chronic ____ ____ requiring dialysis & transplant

A
  • renal failure
135
Q

diabetic nephropathy involves…

A
  • the glomerular capillaries
136
Q

what occurs in the early stages of nephropathy

A
  • loss of negatively charged proteoglycan in the basement membrane allows small amount of albumin to filter into the tubules & enter the urine
137
Q

what is an early sign of nephropathy

A
  • microalbuminuria
138
Q

what occurs later in nephropathy

A
  • glomerulosclerosis

- the process continues, the glomerulus is destroyed & the nephron is lost

139
Q

what is glomerulosclerosis

A
  • fibrosis & thickening of the glomelular capillary basement membrane
140
Q

what does the loss of nephrons cause ?

A
  • the loss becomes so great that renal failure occurs
141
Q

describe treatment of nephropathy

A
  • ACE inhibitors
  • ARBs
  • SGLT2 inhibitors
142
Q

why do we give ACE inhibitors and ARBs for nephropathy

A
  • they provide renal protection

- they decrease glomerular filtration pressure which decreases sclerosis

143
Q

what is macroangiopathy? what does this lead to in diabetes

A
  • disease of large blood vessels

- in diabetes this leads to accelerated atherosclerosis

144
Q

explain why macroangiopathy occurs with diabetes

A
  • remember, with prolonger hyperglycemia, glucose binds to proteins to create advanced glycosylation end-products
  • AGEs within blood vessels capture LDL, activate macrophages & inflammatory cytokines, and promote prolieration of vascular cells
  • all of which accelerate athersclerosis
145
Q

what conditions does macroangiopathy cause?

A
  • prevalence of coronary heart disease is increased 2-4 times higher
  • up to 80% of diabetics will die from athersclerosis related illness
  • increased risk of stroke (CVA) and peripheral vascular disease
146
Q

list 3 ways diabetes can increase the risk of atherosclerosis

A
  1. high levels of BG create AGEs which can damage the endothelium directly & recruit inflammatory cells (macrophages & cytokines)
  2. deficiency in insulin increases blood VLDL & decreases clearance of VLDL. also increases LDL
  3. incidence of hypertension is higher in diabetes
147
Q

describe treatment for macroangiopathy

A
  • statins (to control LDL and VLDL)

- bp meds (ACE inhibitors & ARBs)

148
Q

what is neuropathy

A
  • group of diseases resulting from damaged or malfunctioning of nerves
149
Q

what is the cause of diabetic neuropathy?

A
  • largely unknown
  • believed to be combined consequences of microangiopathy & accumulation of sorbitol within neurons via the polyol pathway
150
Q

how could microangiopathy cause neuropathy

A
  • impairs nutrient delivery to neurons

= demylination & loss of nerve fibers

151
Q

what is sorbitol

A
  • type of sugar
152
Q

what is the polyol pathway

A
  • this is a 2 step process that converts glucose into fructose
    glucose –> sorbitol –> fructose
153
Q

what are 2 types of neuropathy

A
  1. symmetric distal polyneuropathy

2. autonomic neuropathy

154
Q

what causes symmetric distal neuropathy

A
  • demyelination of distal peripheral nerves
155
Q

describe manifestations of symmetric distal neuropathy

A
  • symmetric sensory loss in the lower extremities
  • numbness & tingling often precede parathesia
  • symptoms then move proximally & eventually effect the hands
156
Q

what is stocking distribution

A
  • description of the progression of neuropathy symptoms in the feet which resembles how you could put a on a sock
  • starts at the toes and works its way up
157
Q

what is glove distribution

A
  • description of the progression of neuropathy symptoms in the hands which resembles how you would put on a glove
  • starts at the fingers & works its way up
158
Q

what is autonomic neuropathy

A
  • neuropathy which effects autonomic (SNS or PSNS) innervation of many different systems
159
Q

what are signs of cardiovascular involvement for autonomic neuropathy

A
  • fixed, resting tachycardia

- orthostatic hypotension

160
Q

what are signs of genitourinary involvement for autonomic neuropathy

A
  • incomplete emptying of the bladder which causes overflow incontinence
  • predisposition to a UTI
  • 50% of diabetic men suffer from impotence
  • female sexual dysfunction –> failure to meet orgasm
161
Q

what is incomplete emptying of the bladder due to autonomic neuropathy called

A
  • neurogenic bladder
162
Q

describe glucogan & epi during autonomic neuropathy

A
  • decreased glucagon & epi response to hypoglycemia
163
Q

what is another manifestation of autonomic neuropathy

A
  • exertional hypoglycemia

NURS 2514 (75 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions