DB Lecture Flashcards
criteria for impaired fasting glucose
HgbA1C between 5.7% and 6.4%
i. An autoimmune disease that destroys the pancreatic beta cells that results in the body not producing sufficient insulin
1) Requires exogenous insulin to survive
2) Usually does not present until about 90% of the beta cells have been destroyed
T1DM
ii. Faster onset usually in ages of 20 or younger
1) Usually a thin body habitus
2) Ketosis is very common
T1DM
i. Body is not responding to insulin
1) Have an over abundance of glucose and free fatty acid fail to stimulate the pancreas to secrete insulin
ii. Slower gradual onset in adults
1) Frequently obese
2) Rarely have ketosis
3) Risk factors: obesity (greatest risk factor), genetics, age (insulin production decreases with age)
T2DM
i. Body has a surge of hormones, growth hormone included, and the body cannot release insulin/respond with insulin sufficiently to respond to the increase in blood sugar
ii. See hyperglycemia in the morning and NO hypoglycemia through the night
iii. Management:
1) Increase evening insulin
Dawn phenomenon
i. Rebound response to nocturnal hypoglycemia that results in hyperglycemia in the AM
ii. Patient does have low sugars through the night
iii. Management:
1) Eat a snack before bed
2) Decrease evening insulin
Somogyi Effect
a. Symptoms + random glucose of > 200 mg/dL
b. Fasting plasma glucose of > 126 mg/dL on two separate occasions
c. Plasma glucose of > 200 mg/dL two hours after a 75-g glucose load during an oral glucose tolerance test
d. A1C > 6.5%
diagnostic criteria for diabetes mellitus
Other than the following sx, what are other common sx of DB?
i. Polydipsia
ii. Polyuria
iii. Polyphagia
iv. Fatigue
v. Weight loss
vi. Blurred vision
vii. Fungal infections
viii. Numbness, tingling of hands and feet
MCC of death in diabetic patients is
CAD
manifestations regarding macrovascular complications associated with diabetes mellitus
i. Main problem is accelerated atherosclerosis
1) Increased risk for stroke, MI, heart failure
2) Renal disease
ii. Increased peripheral vascular disease, cerebrovascular disease (strokes)
Macrovascular complications treatments in general
Smoking cessation, daily aspirin, BP control, lipid-lowering agents, strict glycemic control
MCC of end stage renal disease
Diabetic nephropathy
hyaline deposition in one area of the glomerulus —> pathognomonic for DM
Nodular glomerular sclerosis of Diabetic nephropathy
Screening test: Diabetic nephropathy
Microalbuminuria –> shows up in the urine about a year before you’ll find proteinuria on the dipstick
a) Usually see HTN develop between the microalbuminuria to proteinuria stages
Diabetic nephropathy Treatment
1) ACE-inhibitor or ARB –> renal protective as dilates the efferent arteriole of the glomerulus as well to prevent increased glomerular pressure and prevent spillage of proteins
Diabetic retinopathy
1) Microvasculature damages to the vasculature in the eye results in:
a) Cotton-wool spots
b) Hard exudates
c) Retinal hemorrhages
d) Venous dilations
2) Can also see cataracts, retinopathy, and glaucoma show up in these patients
3) Serious complications
a) Vitreal hemorrhage
b) Retinal detachment
MCC of blindness
Diabetic retinopathy - Edema of the macula in the eye
Diabetic retinopathy - Diagnostics
Require ophthalmologist screening yearly
Diabetic retinopathy - Treatment
Laser photocoagulation
1) Usually affects sensory nerves in a “stocking/glove pattern”
2) Usually begins in feet, later involves the hands (longest nerves are always affected first)
3) Lose sensory function of feet and unable to feel pain or ischemia in the feet
Peripheral neuropathy of DB:
Pathophysiology/Clinical manifestations
1) Numbness and paresthesias are common
2) Hypersensitivity to light touch
3) Severe “burning” pain that is worse at night and intolerable
Peripheral neuropathy of DB
Tx of Peripheral neuropathy of DB
1) NSAIDs
2) Gabapentin
3) Pregabalin
4) Duloxetine
5) TCAs
1) Impotence in men is the most common presentation
2) Gastroparesis resulting in chronic nausea and vomiting with early satiety
Autonomic neuropathy of DB:
Pathophysiology/Clinical manifestations
Treatment of gastrparesis
pro-motility agents (metoclopramide)
1) Impaired leukocyte function, reduced blood supply, and neuropathy
2) Impaired wound healing
These are all common complications of what in DB?
Increased susceptibility for infection
Common infections of DB?
a) Cellulitis, candidiasis, pneumonia, osteomyelitis, polymicrobial foot ulcers
b) Increased levels of sugars bring in more yeast/bacteria
1) Secondary to insulin deficiency and glucagon excess that cause accelerated severe hyperglycemia and accelerated ketogenesis
2) Severe hyperglycemia leads to osmotic diuresis = dehydration and volume depletion
DKA
1) Respiratory alkalosis
2) Fruity (acetone) odor on breath
3) Kussmaul’s respirations
4) Volume depletion
5) Polydipsia, polyphagia, polyuria
6) LOC, frank coma
DKA presentation
1) Hyperglycemia: > 450 to 850
2) Metabolic acidosis
3) Ketonemia
4) Hypokalemia (esp. with infusion of insulin due to K+ shift to depolarize the beta cells)
5) Can see falsely negative ketones in urine and serum due to circulatory collapse
DKA diagnostics
1) Insulin
a) DOUBLE CHECK K+
2) Fluids
3) Electrolytes –> potassium
Start 1 to 2 horus after insulin
DKA Tx
1) Low insulin levels lead to hyperglycemia
2) Severely elevated glucose levels cause an osmotic diuresis with ensuing dehydration
a) Prevent ketogenesis through release of low levels of insulin
3) Severe dehydration due to the osmotic diuresis of hyperglycemia
Hyperosmolar hyperglycemic nonketotic syndrome (HHKS) pathophysiology
1) CNS findings and focal neurologic signs are common
2) Seizures
3) Thirst, polyuria
4) Hypotension, tachycardia
Hyperosmolar hyperglycemic nonketotic syndrome (HHKS) presentation
1) Serum glucose > 900
2) Hyperosmolarity with serum osmolarity > 320 mOsm/L
3) NO ACIDOSIS
Hyperosmolar hyperglycemic nonketotic syndrome (HHKS) diagnostics
1) Fluid replacement with normal saline
a) When glucose gets to around 250, add in D51 (glucose water)
2) Insulin IV bolus and then low dose infusion
Hyperosmolar hyperglycemic nonketotic syndrome (HHKS) Treatment
Insulin levels are usually ___ to ____ with T2DM
Insulin levels are usually normal to high with T2DM
