Test 1 Flashcards
1
Q
What does the endocrine system secrete into
A
Secretes hormones into blood
2
Q
What does the exocrine system secrete into
A
Secretes hormones into ducts
3
Q
Pancreas
A
Large diffuse organ
BOTH endocrine and exocrine gland
4
Q
Acini tissue
A
The specialized cells of the pancreas that secrete into ducts
5
Q
Islets of Langerhans
A
Tissue of the pancreas that secretes insulin
1% of the volume of the pancreas but very important
6
Q
Exocrine function
A
Involves synthesis and release of acini
- digestive enzymes
- sodium bicarbonate
Plays essential role in digestion and absorption of food in small intestine
7
Q
Endocrine function
A
Involves synthesis and release of hormones produced in the Islets of Langerhans
Function to regulate glucose levels
- insulin
- glucagon
- somatostatin
8
Q
Cell type for insulin
A
Beta cell
9
Q
Action of insulin
A
Lower blood glucose (or other trad sugars) by allowing it to enter cells
10
Q
Cell type of glucagon
A
Alpha cells.
11
Q
Action of glucagon
A
Increase release of glucose from the liver into the blood
Stimulates glycogenolysis and gluconeogensis
Increases lipolysis and output of ketones by liver
Enhances uptake of AA by liver
MAINTENANCE OF BLOOD GLUCOSE BETWEEN MEALS
Acts in opposite of insulin
12
Q
Cell type of somatostatin
A
Delta cell
13
Q
Action of somatostatin
A
Decrease gastrointestinal activity after ingestion of food > Extended time over which food is absorbed
Inhibits insulin and glucagon > extends use of absorbed nutrients by tissues
14
Q
Maintenance of blood glucose after a meal
A
Glucose levels rise which stimulates insulin to be secreted in response
- glycogenesis
- lipogenesis
15
Q
Glycogenesis
A
2/3 of glucose from the mean is stored in the liver as glycogen
16
Q
Lipogenesis
A
When tissues saturated with glycogen glucose is converted to fatty acids and stored as triglycerides in fat cells
17
Q
Maintenance of blood glucose between meals
A
The liver releases glucose to maintain levels within normal limits
- glycogenolysis
- gluconeogensis
18
Q
Glycogenolysis
A
Glycogen is broken down to release glucose
19
Q
Gluconeogensis
A
Synthesis of glucose from amino acids, glycerol and lactic acid
20
Q
Action of insulin on glucose
A
increase glucose transport into skeletal and adipose tissue
Increase glycogen synthesis
Decrease gluconeogensis
21
Q
Action of insulin on fats
A
Increase glucose transport into fat cells
Increase fatty acids transport into adipose cells
Increase triglyceride synthesis within fat cells
Inhibits adipose cell lipase (break down)
Activates lipoprotein lipase in capillary walls
22
Q
Action of insulin on proteins
A
Increase active transport of AA into cells
Increase protein synthesis by increasing transcription of mRNA and accelerating protein synthesis by rRNA
Decrease protein breakdown by enhancing use of glucose and fatty acids as fuel
23
Q
HDL
A
High density lipoproteins
(Good cholesterol)
24
Q
LDL
A
Low density lipoproteins
(Bad cholesterol)
25
Diabetes and lipoprotein lipase
Causes not enough activation of lipoprotein lipase so there is an exceleration of atherosclerosis
^ cholesterol ^ triglycerides ^ LDL and decreased HDL
26
The major action of insulin on tissues
Decrease blood glucose by allowing it to enter cells
27
Anabolic action of insulin on tissues
Promotes synthesis of proteins, CHOs, lipids, nucleic acids in live, muscle and adipose
28
Action on insulin on the liver
Stimulates:
- synthesis of glycogen and increased uptake
- fatty acids synthesis
Inhibits:
- Glycogenolysis
- gluconeogensis
- ketogenesis
29
Action of insulin on muscle
^ uptake of glucose and AA
^ glycogen and protein synthesis
Inhibits protein catabolism
30
Action of insulin on adipose tissue
Increased glucose uptakr and fat synthesis (lipogenesis)
Decreased fat breakdown (by inhibiting adipose cells lipase)
31
Action of insulin on K+
Increases K+ uptake by cells which is needed for aj or cardiac conduction
32
Action of insulin on lipids
Metabolism of plasma lipids and lipoproteins WNL tangles
33
GIK mechanism
1) blood glucose levels increase
2) insulin moves the glucose intracellularly
3) K+ hitches a ride and also moves intracellularly
34
Hypoglycemia
Can be caused by excess insulin
Decreased blood
35
S/s of hypoglycemia
Hunger
Tremor
Sweating
Weakness
Malaise
Irritability
Mental changes
Coma > DEATH
36
Hyperglycemia
Can be caused by a insulin deficit
increased blood glucose
37
S/s of hyperglycemia
Polydipsia - thirst
Polyphagia - hunger
Polyuria - UO
Dehydration
Fatigue
Mental changes
Coma > DEATH
38
Action of glucagon on glucose
Promotes breakdown of glycogen into glucose phosphate
Increase gluconeogensis (synthesis of glucose)
39
Action of glucagon on fats
Enhances lipolysis in adipose tissue > liberates glycerol for the use in gluconeogensis
Activates adipose cell lipase
Enhances lipolysis in adipose tissue > liberates fatty acids (so they can be used for energy) > ketones produces as a waste product
40
Action of glucagon on proteins
Increases breakdown of proteins into AA for use in gluconeogenesis
41
What produces catecholamine
The adrenal gland
- epinephrine and norepinephrine
42
Function of catecholamines
Maintain blood gloves levels *during stress*
- mobilizes glycogen stores
- decreases movement of glucose into body cells (keep levels high in blood)
- inhibits insulin release from beta cells
- mobilizes fatty acids from adipose tissue
43
Catecholamines and hypoglycemia
Is an important homeostatic mechanism meant to conserve glucose
44
Function of growth hormone
- Increase protein synthesis in ALL cells of body
- Mobilizes fatty acids from adipose tissue (to be used for fuel)
- Antagonizes the effects of insulin
- decreases cellular uptake and use of glucose > increases blood glucose by as much as 50-100% > stimulates further insulin secretion
45
Growth hormone is inhibited by
Insult and increased levels of blood glucose
So there isn’t a prolonged effect of elevated GH
46
Things that increase Growth Hormone
Fasting (and hypoglycemia)
Exercise
Stress: anesthesia, fever, trauma
47
Paths of growth hormone production
Hypothalamus > GHRH > Anterior Pituitarty > GH
Hypothalamus > Somatostatin > Anterior Pituitary > GH
48
Where are Glucocorticoid Hormones synthesized
Adrenal Cortex
- cortisol (hydrocortisone) responsible for 95% of activity
49
Action of Glucocorticoid Hormones
Regulate metabolism of glucose
- critical to survival during periods of fasting and starvation
Stimulate gluconeogensis by the liver (^ production 6-10x)
Moderately decrease use of tissue glucose
50
What causes levels of glucocorticoid hormones to increase
Stress: infection, pain, trauma, surgery, prolonged strenuous exercise, acute anxiety
Hypoglycemia
51
GLP-1 and where it is released
Glucagon-like peptide-1
Released in distal small bowel
52
GIP and where it is released
Glucose-dependent insulinotropic polypeptide
Released in jejunum
53
Action of GLP-1 and GIP
Incretin hormones released from gut USED TO MANAGE DIABETES AND WEIGHT LOSS
Signal beta cells to increase insulin secretion and decrease alpha cells’ release of glucagon
GLP-1 also slows down the rate at which food empties from the stomach and acts on the brain to increase satiety
54
Amylin and its release
Seminal to somatostatin
Released along with insulin from beta cells
55
Action of Amylin
Has much of the same effect as GLP-1
- Decreases glucagon levels, which will then decrease the liver’s glucose production
- slows the rate at which food empties from the stomach
- acts on the brain to increase satiety
56
Diabetes definition
Disorder of carbohydrate, protein and fat metabolism
“The running through of sugar”
57
Cellular level causes of diabetes
Involves absolute or relative insulin deficiency and/or insulin resistance
- absolute deficiency: beta cells not making any
- impaired release of insulin by pancreatic beta cells
- inadequate or defective insulin receptors
- production of inactive insulin
- insulin is destroyed before it carries out its action
58
Cellular effects of diabetes
Cannot carry glucose into fat and muscle cells > cellular starvation > breakdown of fat and protein
59
Characteristics of Type 1 diabetes
Absolute insulin deficiency
60
Etiology of type 1
Autoimmune
Idiopathic
61
Treatment of type 1
Insulin
62
Characteristics of type 1.5
Some of both type 1 and 2
63
Etiology of type 1.5
Latent autoimmune diabetes in adults
64
Treatment of type 1.5
Oral meds at first
Insulin within 5 yrs
65
Characteristics of type 2
Insulin insensitivity
Insulin secreting deficiency
Inappropriate gluconeogensis
66
Etiology of type 2
Obesity
Genetics (stronger in type 2 than 1)
67
Treatment for type 2
Diet
Exercise
Hypoglycemics
Transporter-stimulators
68
Etiology of other specific types of diabetes
Malnutrition
Corticosteroids
(Treatment is based on cause)
69
Characteristics of GDM
Gestational diabetes
70
Etiology of GDM
Increased metabolic demands
71
Treatment for GDM
Diet
Metformin
Insulin
72
Onset of type 1
Any age
Usually < 30
73
Onset for type 1.5
> 30
74
Onset for type 2
Usually after 40
8/10 obese
75
Pathophysiology of type 1
NO insulin production
76
Pathophysiology of type 1.5
Damage to beta cells
Genetic factors
Possibly insulin resistance
77
Pathophysiology of type 2
Produce insulin BUT not enough or tissues are resistant
78
Major complications of type 1
DKA (cell starvation)
79
Major complications of type 1.5
DKA
80
Major complications of Type 2
HHNK (less ketosis)
81
Manifestations type 1
Hyperglycemia
Glucosuria - bc nephrons can’t filter it all (overwhelmed)
Symptoms develop more acutely
3Ps: polyuria, polydipsia, polyphagia
Weight loss despite norm or increased appetite
- osmotic diuretics, vomiting d/t ketoacidosis
- cells must use stored CHOs, fats and proteins for energy
Other:
- recurrent blurred vision
- fatugue
- paresthesias
- recurrent skin infections
82
Manifestations of type 2
Hyperglycemia and glucosuria
Symptoms develop more insidiously (over time) - bc still some insulin production
Only 2Ps: polyuria and polydipsia (may be overlooked bc no ketoacidosis bc glucose ^ is gradual) NOT polyphagia
Obesity
Other:
- recurrent blurred vision d/t hyperosmolarity
- weakness and fatigue d/t lowered plasma volume
- paresthesias d/t dysfunction of peripheral sensory nerves
- chronic skin infections
83
Casual or Random Plasma Glucose
Diagnostic tool
Given ANY time of day without regard to time since last meal
Not very useful
84
Fasting Plasma Glucose (FPG) or 2-hour PG
Diagnostic tool
Once preferred d/t ease of admin, convenience, acceptability to patients and lower cost
FPG < 126 mg dL is normal
Fasting defined as no caloric intake for at least 8 hours
2 hour PG diagnosis more people with DM then FPG
85
Oral Glucose Tolerance Test (OGTT)
Diagnostic tool
Usually used in pregnant people
24-28 weeks gestation and 6-12 weeks postpartum if +
Uses 75 g glucose dissolved in water
Measurements at fasting, a hour and 2 hour
NOT recommended for routine use just for gestational diabetes
86
Diagnosis of GMD with OGTT
Fast ≥ 92 mg/dL
1 hour ≥180 mg/dL
2 hour ≥ 153 mg/dL
> means its a concern
87
Glycated or Glycosylated Hemoglobin (HgA1c)
Diagnostic tool and tool for measuring how one is managing
Amount of blood glucose bound to hemoglobin is directly proportional to the amount of clucose exposure over 120-dat lifespan of RBC
Reflects average blood glucose levels for 2-3 months prior to test
88
Glycohemoglobin
Blood glucose bound to hemoglobin
89
HgA1c results
Ideal < 5.7
Moderate: 5.7-6.4
Poor: ≥ 6.5
90
Goals for blood glucose monitoring
HgbA1C maintained at 7% or less
Majority of preprandial blood glucose levels 80-120 mg/Dl
Bedtime blood glucose between 100-140 mg/dL
91
Urine Glucose Test
Ease of blood glucose monitoring has made this almost obsolete
ONLY reflects urine glucose levels
Influenced by: renal threshold for glucose, fluid intake and urine concentration, urine testing method and drugs
92
Urine Ketones test
Remains an important part of monitoring diabetic control especially type 1 who are prone to DKA bc ketones are produced by breaking down fats into acids
93
C-Peptide Assays
Reliable indicator for pancreatic beta cell function
Strong coordination w/ insulin and C peptide levels
Measurements before and after glucagon stim may be valuable for assessing diabetic insulin therapy
*Helps to delineates type 1 from type 2
Also monitors recovery after excision of insulinoma (rising levels of C-peptide suggests recurrence or metastasis)
94
Insulinoma
Timer in pancreas that overproduces insulin
95
What is C-peptide
Proinsulin (inactive) breaks into insulin (active) and the c-peptide which stays in the blood
Measuring can tell if someone is type 1 diabetic
96
Categories for increased risk for diabetes
Impaired fasting glucose (IFG): FPG = 100-125
Impaired Glucose Tolerance (IGT): 2 hour PG in OGTT= 140-199 mg/dl
**A1C =5.7-6.4%
97
A1C ranges
Normal: <5.7%
Pre diabetic: 5.7-6.4%
Diabetic: ≥ 6.5%
98
Metabolic Syndrome “Syndrome X”
Presence of any 3 of the following:
Central obesity “apple shape”
Fasting serum triglycerides > 150 mg/dL
Low HDL cholesterol:
- men < 40 mg/dL
- women < 50 mg/dL
Blood pressure ≥ 130/85
Fasting glucose ≥ 110 mg/dL
99
Additional s/s of “syndrome x”
Elevated uric acid levels
Associated diseases and signs are:
- fatty liver
- progressing to non-alcoholic fatty liver disease
- polycystic ovarian syndrome
- hemochromatosis (iron overload)
- acanthosis nigricans (skin condition featuring dark patches)
100
Gestational Diabetes prevalence
Occurs in about 7% of pregnancies
50% with family Hx, glycosuria, Hx stillbirth/spontaneous abortion, fetal abnormalities or LGA baby, obese, advanced maternal age, > 5 pregnancies
101
Why is management of gestation diabetes critical
Increased risk complications, mortality, fetal abnormalities including macrosomia, hypoglycemia, polycythemia, hyperbilirubinemia
102
Tax for gestational diabetes
Blood glucose monitoring: fasting + postprandial
Nutritional guidance > normoglycemia, proper weight gain, avoid ketosis
103
Gestational diabetes
Develop DM during pregnancy
type 1 DM discover during pregnancy and undiagnosed asymptomatic type 2 DM discovered during
Most: norm glucose first half > develop relative insulin deficiency during second half
Most resolve but ^ risk of type 2 later
104
GDM Risk assessment
Should be undertaken at first prenatal visit
Women with clinical characteristics consistent with risk of GDM should undergo glucose testing asap
Ig they are found not to have it at initial screening they should retest between 24-28 weeks
Women of average risk should be tested at 24-28 weeks
105
Therapeutic goals of treatment
Maintenance of near norm blood glucose levels
Achievement of optimal lipid levels
Adequate calories to attain and maintain reasonable weight
Treatment and prevention of chronic complications
Improvement of overall health
106
Nutrition therapy for type 1
Based on individuals usual food intake
- should eat at consistent times synced with the time action of insulin prep used
- need to monitor blood glucose and adjust insulin doses for amount of food usually eaten
Intensified insulin therapy such as multiple daily injections or use of an insulin pump allows considerable flexibility in what and what they eat
107
Nutrition therapy for type 2
Hypo-caloric diets and weight loss
- usually improve short term glycemic levels and have the potential to improve long term metabolic control
- BUT no one proven strat or method that can be uniformly recommended
Moderate caloric restriction ( lower than 250-500 cal) and nutritionally adequate meal plan
- reduction of total fat, especially saturated
Spacing of meals and spreading carbohydrate intake throughout the day
May require require addition of oral hypoglycemic (or insulin)
108
Benefits of exercise treatment
Improved glucose tolerance
Weight loss or maintenance of desired body weight
Improved cardiovascular risk factors
Improved response to pharmacological therapy
Improved energy level, muscular strength, flexibility, quality of life and sense of well-being
109
Medication treatments
Insulin
- insulin is destroyed in the GI tract > must be administered by injection
- categorized according to onset, peak and duration of action
- four types: rapid, short, intermediate, long acting
- pumps used only for rapid
- injectable protocols need to be taught
Oral agents
Injectable non-insulin meds
110
Pancreatic transplant treatment
Can restore carbohydrate metabolism to normal
Require immunosuppression
Not lifesaving BUT can sig improve quality of life
111
Survival rates for pancreas transplants
Individual: 1 yr=90% 3 yrs = 80%
Graft: 1 yr = 72% 3 yr = 57%
112
Diabetic Ketoacidosis
Acute complication that occurs primarily with Type 1 and can happen in type 1.5
Acute insulin insufficiency with life-threatening and dramatic pres
113
Hyperosmolar Hyperglycemia Non-Ketotic Coma/Syndrome
Acute complication that occurs primarily with type 2 (often no previously diagnosed)
Relative insulin insufficiency with 50% mortality
Cannot dev DKA bc have insulin
114
Somogyi effect
Unrecognized hypoglycemia at night >
increased catecholamines, glucagon, Cortisol, & GH >
hyperglycemia in AM >
Increased exogenous insulin >
More hypoglycemia >
Vicious cycle
115
Dawn Phenomenon
Acute complication of diabetes
Pre-dawn hyperglycemia w/out antecedent hypoglycemia (blood sugar normal > at dawn body releases stored glucose)
May be d/t changes in circadian rhythms
Liver gives an early-AM “snack”
GH a possible factor
116
Hypoglycemia
Acute complication of diabetes
117
Hyperglycemia effects
Increase in blood glucose > increase in blood osmolarity > cellular dehydration (shrinking) and renal threshold exceeded (which causes osmotic diuretics) > dehydration > thirst, ^ HR, warm and dry skin
118
Onset of DKA
1-24 hours
119
Presenting Hx of DKA
One to several days of polyuria and polydipsia
N&V, anorexia and acute abdominal pain
120
Precipitating factors of DKA
Failure to take insulin
Infection or other illness
Trauma or physical stress
Emotion stress & extreme anxiety
Pregnancy
Continuous insulin pump failure
121
Pathophysiology of DKA
Inadequate insulin hinder glucose uptake by fat and muscle cells
Glucose accumulates in blood
Liver responds to starving cells by converting glycogen to glucose and releasing into blood further increasing blood glucose
When renal threshold exceeded > excess glucose excreted in urine
Rapid metabolism of protein for energy
Loss of intracellularly K+ and P and excessive liberation of AA
Liver convers AA to glucose and urea
Blood glucose evens grossly elevated
Increased serum osmolarity and glucosuria > osmotic diuresis > dehydration
122
DKA Pathophysiology part 2
Cells convert fats into glycerol and fatty acids for energy
Fatty acids cannot be metabolized at same rate of release
Fatty acids accumulate in the liver and converted into ketones
Ketones accumulate in the blood & urine and cause acidosis
Acidosis leads to more tissue breakdown, more ketosis, more acidosis which leads to shock coma and death
123
The deadly cycle of DKA
> decreased glucose excretion > further increase blood glucose levels > hyperosmolarity and dehydration > shock, coma, death
124
Physical manifestations of DKA
Dehydration
- warm, dry skin
- dry mucous membranes
- acute weight loss
- tachycardia
- weak threads pulse
- hypotension
Ketoacidosis
- anorexia, N&V
- acetone breath
- abdominal pain
- decreased CNS > lethargy, fatigue, stupor, coma
125
Compensation manifestations of DKA
Tachypnea and Kussmaul respiration (fast and deep)
126
Lab results for DKA
*Serum glucose: 250-600 mg/dL
*Glucosuria
*ABGs: pH < 7.3, bicarbonate < 15 mEq/L
* ketonemia & ketonuria
Increased BUN d/t dehydration
K+ high, low, or normal depending on degree of dehydration and acidosis
127
Treatment of DKA
Fluid replacement
- deficits of 5-8 L > give 1-2 L of NS over 1-2 hrs
IV regular insulin
- continuous drip or bolus
K+ replacement once UO re-establishes
Bicarbonate
- in pH < 7.2, but give cautiously bc of CNS acidosis
5% dextrose added when glucose < 250
128
Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNK) onset
Insidious
129
Presenting Hx of HHNK
Polyuria for several weeks or days
130
Precipitating factors of HHNK
Conditions that stress insulin tolerance: peritoneal dialysis, hemodialysis, tube feeding, TPN
Elderly with renal insufficiency
Drugs: steroids, diuretics, Dilantin
Infection, CVA
131
Physical manifestations of HHNK
Severe dehydration:
- dry mucous membranes
- extreme thirst
Neurologic:
- depressed sensorium lethargy > coma
Neurologic deficits:
- + Babinski’s
- paresis or paralysis
- sensory impairment
- hyperthermia
- hemianopia
132
Laboratory manifestation of HHNK
Serum glucose > 600 mg/dL
Serum osmolarity > 300 mosm
Glucosuria
Increased BUN d/t dehydration (hypovolemia and decreased renal perfusion)
Na+ and K+ WNL
Decreased bicarbonate d/t lactic acidosis from hypovolemia
NO KETOSIS
133
Treatment of HHNK
Restore intravascular volume with NS
Continuous IV insulin
K+ replacement
134
Complications of HHNK
Thrombosis (from Hyperosmolar blood that is more sticky due to dehydration) - blood is thickening due to lack of fluids
Embolus
Pneumonia - breathing impaired w/ coma
ARDS
135
Manifestations of Hypoglycemia
Glucose < 50 mg/dL
ANS Response:
- parasympathetic: hunger, nausea, hypotension, bradycardia
- sympathetic: anxiety, sweating, vasoconstriction, tachycardia
Neuroglycopenia:
- altered cerebral function d/t brain starvation
- headache, vagueness, decreased problem-solved, slurred speech, emotional lability, convulsions, coma
136
At risk for hypoglycemia
Tight control, pump or multiple injections
* beta blockers d/t no sympathetic effect
Autonomic neuropathy
Oral hypoglycemic agents
Type 2 w/ excess insulin secretion
Error in insulin dose
Not enough food
Increased exercise
Failure to decrease insulin as infection or other stress resolves
137
Tx for Hypoglycemia
Immediate ingestion of CHO
Glucagon IV, SQ, IM - pancreas tells liver to release glycogen (stored glucose)
138
What does it mean if dawn phenomenon is seen alone
Mild hyperglycemia
139
What does it mean if dawn phenomenon is seen in combo with somogyi effect
Profound hyperglycemia
140
Tissues MOST affected by elevated blood glucose
Body cells NOT dependent on insulin to use glucose > most affected by chronically elevated blood glucose levels
RBCs
Glomerular cells
Central & peripheral nerves
Blood vessel cells
141
Chronic macrovascular problems of diabetes
CV Disease
Cerebrovascular Disease
Peripheral Vascular Disease (PVD)
142
Chronic microvascular problems of diabetes
Diabetic nephropathy
Diabetic neuropathy
Diabetic retinopathy
Erectile dysfunction
143
Hyperglycemia injury to the heart
(Macrovascular issues)
Coronary artery disease
- coronary syndrome
- MI
- CHF
144
Hyperglycemia injury to the brain
(Macrovascular issues)
Cerebrovascular disease
- TIA
- CVA
- Cognitive impairment
145
Hyperglycemia injury to extremities
(Macrovascular issues)
Peripheral vascular disease
- ulceration
- gangrene (necrosis)
- amputation
146
Hyperglycemia injury on the eyes
(Microvascular issues)
Retinopathy
Cataract
Glaucoma
>>> blindness
147
Hyperglycemia injury to the kidneys
(Microvascular issues)
Nephropathy
- Microalbuminuria
- Gross albumunuria
>> kidney failure
148
Hyperglycemia injury to the nerves
(Microvascular issues)
Neuropathy
- peripheral
- autonomic
>> amputation
149
Somatic peripheral neuropathy
Polyneuropathies
Mononeuropathies
Amyotrophies
150
Characteristics of polyneuropathies
Paresthesias
Impaired sensation
Diminished reflexes
151
Characteristics of mononeuropathies
Involvement of a mixed nerve trunk
Motor AND sensory nerves affected
152
Characteristics of amyotrophies
Muscle weakness and wasting
153
Characteristics of autonomic neuropathies
Impaired vascular function
- postural hypotension
Impaired GI function
- gastric atony
- diarrhea
Impaired GU function
- paralytic bladder
- incomplete voiding
- impotence
- retrograde ejaculation
Cranial nerve involvement
- extraocular nerve paralysis
- impaired pupil responses
- impaired special senses
154
Cardiovascular disease
Diabetes can cause it and its a major cause of death
Accelerated atherogenesis
- onset earlier age
- progression more rapid
- manifestations more severe
Hyperlipoproteinemia
- HDLs lower in uncontrolled DM
Abnormal platelet function
155
Management of CVD
Diet, weight loss, exercise, quit smoking, control HTN
156
CVD and DM
40 yr old w/ diabetes > 1/2 risk of CVD if no smoking, normal cholesterol and not HTN
- + HTN > 2x risk
- + high cholesterol > 8x risk
- + smoking > 11x risk
157
Eye Disease and DM
Can be caused by DM
Retinopathy > leading cause of blindness
Incidence is greater in type 1
Glaucoma
Cataracts
Blurred Vision
158
Non-proliferative “background” retinopathy
Retinal veins tortuous and dialated
Exudates contain lipoproteins, hemorrhages, scarring, retinal detachment
159
Proliferative “neovascularization” retinopathy
Traction on vitreous > detachment
160
Treatment for proliferative retinopathy
Laser surgery to destroy new blood vessels and stop hemorrhages
Vitrectomy
161
Glaucoma
Laser surgery to destroy new blood vessels and stop hemorrhages
Vitrectomy
162
Blurred vision and DM
D/t osmotic changes
Takes 6-8 weeks to resolve
163
Nephropathy and DM
Early:
Kidney hypertrophies
^ GRF and albuminuria in new onset Type 1
164
Early:
Kidney hypertrophies
^ GRF and albuminuria in new onset Type 1
