diabetes complications Flashcards
ACUTE COMPLICATION OF DM
HYPOGLYCEMIA
DIABETIC KETOACIDOIS (DKA)
HYPERGLYCEMIC HYPEROSMOLAR SYNDROME (HHS PREVIOUSLY KNOWN AS HHNK)
IMPORTANCE OF GLUCOSE
Glucose is the fuel that provides energy for cells
Insulin dependent cells for glucose transport
Adipose tissue
Skeletal muscles
Without insulin → Cellular starvation
HYPOGLYCEMIA: BG #
BG <70
Treatment of Hypoglycemia - rule of 15
Rule of 15”
At first sign, 15g of PO simple carb
15g simple sugar (5-6 hard candies, 3 glucose tabs), 4-6 oz apple or orange juice or a regular soda
If hypoglycemia persists after 10-15 minutes, repeat x 2-3. Call PCP if no improvement
Treatment of Hypoglycemia - if inpatient -
Inpatient:
12.5 to 25gm (25-50mL) Dextrose 50% IVP if NPO
Hypoglycemic Unawareness**- and who gets it?
body doesn’t signal when hypoglycemia is occuring
When a person lacks the autonomic nervous system triggers to hypoglycemia
Usually found in people with long-standing DM I, frequent episodes of hypoglycemia and older people**
Diabetic Ketoacidosis (DKA) - is it fast or slow?
Usually occurs with DM1 but can occur with DM2 in severe illness or stress when the pancreas cannot meet the extra insulin demand
Occurs abruptly
DKA - patho - 1
(dik is 1 fat ketone)
Profound insulin deficiency
Metabolism of fat storage resulting in ketone byproducts → ketoacidosis → metabolic acidosis
dka - s/sx - the Ps
3Ps: Polyuria, Polydipsia, Polyphagia
DKA: LAB FINDINGS - BG (DKA in the year 300)
BG > 250-300mg/dl
DKA: TREATMENT = CORRECT DEHYDRATION - and what number to give dextrose?
THREE TARGETS:
CORRECT DEHYDRATION:
Fluid replacement
Start with 1/2NS or NS to achieve staple BP. Then IVF with dextrose when BG approaches 250 mg/dl to prevent hypoglycemia
HYPEROSMOLAR HYPERGLYCEMIC SYNDROME (HHS) - what is BG?
Severe hyperglycemia > 600 mg/dl
HHS: causes
Etiology:
HHS less common than DKA
Infection: UTI, PNA, sepsis, pancreatitis
Elderly > 60 yrs old
Neglected DM
Undiagnosed DM
HHS often related to impaired thirst sensation and/or functional inability to replace fluids
Lab values:
BG > 600mg/dL
HHS : TREATMENT- monitor for what with IV fluids?
Large volumes of fluid replacement with NS or ½ NS is priority
Insulin infusion
Monitor for signs of fluid overload
Pulmonary edema (SOB, ↑O2 requirement, DOE, orthopnea, anxiety, pink frothy sputum)
Monitor cardiac and renal function
Electrolyte replacement
Correct precipitating factor
Complications of chronic uncontrolled diabetes
ANGIOPATHIES
MACROVASCULAR COMPLICATION:
Large and medium sized blood vessels
Increase risk for: CAD, CVA, PVD, HTN
MICROVASCULAR COMPLICATION:
From long standing diabetes over 10-20 years
Neuropathy
Retinopathy
Nephropathy
Skin changes
NEUROPATHY
SENSORY NEUROPATHY: OCCURS IN 60-70% OF PATIENTS
Distal symmetric polyneuropathy affecting both hands and feet
PVD and PAD
Abnormal sensation: paresthesia, tingling, burning, itching
AUTONOMIC NEUROPATHY: AFFECTS ALL BODY SYSTEMS
Hypoglycemic awareness
Urinary retention and bowel incontinence d/t ↓ sensation of bladder and colon walls
Gastroparesis: anorexia, n/v, Gerd, persistent feeling of fullness
Cardiovascular: postural hypotension, silent/painless MI
Sexual dysfunction
NEPHROPATHY
Glomerular basement membrane thickening
Damage to small blood vessels of the glomeruli: glomerular sclerosis
Leading cause of ESRD (end stage renal disease) in U.S.; Occurs in 20-40% of diabetics
RETINOPATHY
Most common cause of new adult blindness
Microaneurysm of the small blood vessels in the retina
Mild to total vision loss depending on the area of aneurysm
Neovascularization occurs but new vessels are very fragile and prone to hemorrhage
INTEGUMENTARY = Acanthosis nigricans
Acanthosis nigricans – velvety light brown or black skin thickening
Manifestation of insulin resistance
Appears on neck, axillae, flexures
INFECTIONS
More susceptible to infections due to impaired mobilization of WBC and phagocytes
High levels of sugar brew more bacteria
Candida Albicans
Slow wound healing
Bladder infections d/t glycosuria and neurogenic bladder
Angiopathy prevents or delays immune response
Education:
Hand hygiene
Personal hygiene
Annual vaccine
Pneumococcal vaccine
DKA - what is the pH?
metabolic acidosis - low pH
hypoglycemia - symptoms
Autonomic:
Shaking, diaphoresis, tachycardia, pallor
hypoglycemia symptoms - CNS
CNS involvement:
slow thinking
slurred speech
blurred vision
dizziness
irrational behavior
seizure
alerted mental status
hypoglycemia - rule of 15 = Once BG improves (and what number)
Once BG improves, usually >120 mg/dL eat bread or 8 oz. milk to prevent rebound hypoglycemia
what carbs to give for the 15 min rule?
(5-6 hard candies, 3 glucose tabs), 4-6 oz apple or orange juice or a regular soda
treatment of hypoglycemia - if pt has no IV access or unconscious
Pt with no IV access and unconscious:
Glucagon IM in deltoid muscle (best absorption)
Nausea common after injection. Turn unconscious person to side to prevent aspiration
Assess cause for person’s hypoglycemia. Further teaching may be warranted to prevent future episodes
what meds contribute to hypoglycemic unawareness?
Use of beta blockers may contribute to hypoglycemic unawareness (masks tachycardia)
what causes diabetic ketoacidosis
Illness, fasting, infection, decreased insulin dosage, undiagnosed Diabetes
DKA patho - 2 (just hyperglycemia)
Gluconeogenesis (process of glucose production from non-carbohydrate source: fats and proteins) → hyperglycemia
DKA patho - 3 - what hormones?
Elevation of counter regulatory hormones → hyperglycemia
Glucagon
Cortisol
Growth Hormone
Catecholamines
DKA - dehydration and BP
Dehydration: poor skin turgor, dry mucosa, tachycardia, hypotension
DKA - neuro & GI
(dik is weak and confused)
Neuro: lethargy, weakness, confusion
GI: abdominal pain, anorexia, vomiting
DKA - respiratory
Respiratory: Kussmaul respiration (rapid deep breathing in response to acidosis, acetone breath)
DKA - PH - what number?
PH < 7.3 (normal 7.35 – 7.45)
DKA - Bicarb (dik was bi before 16)
Bicarb < 16 (normal 25-35)
DKA - serum osmolality (think dehydration)
Positive serum and urine ketones
↑ serum osmolality (solutes in the plasma)
DKA - Na+, Phos
↓ Na+, Phos (too much sugar in plasma pushes out sodium)
DKA - K+
Normal to ↑ K+ (pushes K out of cells)
(K moving out of cell into vasculature in exchange for H+)
DKA - WBC and BUN
Potential ↑ WBC, ↑ BUN
Insulin independent cells (the big ones)
Insulin independent cells for glucose transport
Brain, liver, kidney, RBCs, eyes, nerve cells, GI
DKA treatment - CORRECT ACIDOSIS - (the same)
CORRECT ACIDOSIS:
IV insulin drip start at 0.1 unit/kg/min (**waste 20mL of insulin when priming tubing-insulin sticks to plastic tubing)
Lower the BG slowly to prevent cerebral edema
Goal 36-56 mg/dl per hr reduction
DKA treatment - CORRECT ELECTROLYTE IMBALANCES - what about K+?
CORRECT ELECTROLYTE IMBLANCES:
Check K+ before initiation of insulin drip
Replete hypokalemia as needed since insulin drives K+ into cells worsening hypokalemia
Bicarb: rarely used unless pH <7
Replete other electrolytes as needed
HHS - serum hyperosmolarity
↑ serum hyperosmolarity (blood more concentrated due to a loss of water)
HHS - NEUROLOGICAL MANIFESTATION:
NEUROLOGICAL MANIFESTATION: somnolence, coma, seizures, hemiparesis, aphasia.
HHS - fast or slow?
(his is slow)
Occurs gradually; Mortality rate of 8-10%
HHS - ketones?
***Usually no ketones present because DM2 make some insulin
HHS - dehydration?
Profound dehydration from osmotic diuresis
HHS - what # is serum osmolality? arterial pH? (HS was my fav number)
***No ketones, arterial pH normal
Serum osmolality > 330 mOsm
neuropathy - albumin and blood? and meds? (just think BP)
MAJOR MANIFESTATIONS ARE:
Albuminuria
Hematuria: less often
Progressive chronic kidney disease
Blood pressure control with ACE-I or angiotensin II receptor antagonist delays progression of kidney damage
Diabetes-related dermopathy (derm is red)
Diabetes-related dermopathy – reddish brown, round or oval patches on shins but also in other areas of the body
Starts scaly, then flattens and becomes indented
Necrobiosis lipoidica diabeticorum
(diabetes necrosis is yellow)
Necrobiosis lipoidica diabeticorum – red-yellow lesions, shiny and transparent revealing tiny blood vessels
what meds cause DKA? (cort and thia cause dik)
corticosteroids, thiazides
