DM - Complications part 4 - Exam 4 Flashcards
What BS level is considered hypoglycemia? Is it mc in T1DM or T2DM?
Associated with plasma glucose < 60 mg/dL
More prominent s/s occur at <55 mg/dL; severe CNS glycopenia s/s at <50 mg/dL
Hypoglycemia is a result of ____ release and ______
epinephrine
neuroglycopenia
What is the body’s physiologic response when the blood glucose in within the ranges listed below:
80-85 mg/dL
65-70 mg/dL
**What is important to note?
80-85 mg/dL - Decreased insulin secretion
65-70 mg/dL - Increased glucagon secretion
65-70 mg/dL - Increased epinephrine secretion
Must have a normally functioning liver for response!
_____ and ____ are increased if hypoglycemia has lasted several hours
Increased cortisol and growth hormone
**If fingerstick glucose is ____mg/dL at time of symptoms, or venipuncture glucose is ____mg/dL at time of symptoms, an underlying hypoglycemic disorder is unlikely!!
80+
65+
What are some common culprits behind DM medication related hypoglycemia?
exogenous insulin
insulin secretagogues such as sulfonylureas, meglitinides - can cause oversecretion of insulin
What 3 ways does insulin promote lower levels of BS?
↑ glucose uptake by peripheral tissues
↑ synthesis of glycogen
↓ glucagon secretion, gluconeogenesis, and glycogenolysis
What are some non-DM medication causes of hypoglycemia? What is the major one?
alcohol
BBs, ACEIs, quinolones, quinine
Why does alcohol cause hypoglycemia?
inhibits hepatic gluconeogenesis
What are the 5 guidelines for DM who consume alchol?
- Warn of risk of hypoglycemia, especially if on a med that also increases hypoglycemia risk
- Educate that symptoms of excess ETOH intake and hypoglycemia can mimic each other
- If carb-counting, do not replace food with alcohol in meal plan
- Encourage light drinking and to stay within recommended guidelines for age/gender
- Choose light beers, calorie-free mixers
What are 4 severe illness that can cause hypoglycemia? What is the major one?
Sepsis
Chronic kidney disease
Chronic liver disease
Malnutrition
Why does sepsis cause hypoglycemia? What can make it worse?
cytokine-accelerated glucose use and inhibited gluconeogenesis
if pt has end-organ failure (liver, kidney) due to septic shock
Why does chronic kidney dz cause hypoglycemia? Chronic liver dz?
not fully understood; thought to be due to impaired renal gluconeogenesis and impaired renal clearance of insulin
impaired hepatic gluconeogenesis, impaired response to increased glucagon and epinephrine secretion
Why does malnutrition cause hypoglycemia?
decreased substrates for gluconeogenesis, glycogenolysis
Hypoglycemia is primarily seen in patients with _____ due to one of multiple causes: (Give 3 causes)
cortisol deficiency
Primary adrenal insufficiency (Addison’s)
Secondary adrenal insufficiency (Hypopituitarism, isolated ACTH deficiency)
Tertiary adrenal insufficiency (Hypothalamic dysfunction)
What are two ordinary actions of cortisol?
Promotion of hepatic gluconeogenesis
Inhibits peripheral tissue utilization of glucose
↓ expression of GLUT (especially GLUT-4)
Loss of ____ activity inhibits the body’s ability
to fully respond to hypoglycemia state, especially in pts with _____
cortisol
comorbid DM
____ is the MC tumors arising from the Islets of Langerhans. What fails as a result?
Insulinoma
Often fail to respond to normal feedback mechanisms to regulate insulin
An insulinoma results in the loss of the first 2 “lines of defense” in our counterregulatory mechanisms. What are they and why are they happening?
Release of glucagon and insulin is very dependent on each other!
Failure of body to decrease insulin
secretion in response to falling glucose
Insulin suppresses glucagon secretion
→ failure of body to secrete glucagon
aka insulinoma is telling the body to constantly produce insulin even when the BS is low thus resulting in hypoglycemia AND insulin suppressed the release of glucagon so when the BS levels start to fall in the body glucagon is inhibited and the BS levels stay low
name 2 scenarios in which hypoglycemia can be seen as reactive
commonly seen after gastric sx and with occult diabetes mellitus
What is dumping syndrome? What is the tx?
abdominal cramps, N/V/D, weakness, dizziness 10 min - 3 hrs after eating
Caused by large dump of sugary/starchy foods into the intestine all at once
Can lead to large release of insulin → hypoglycemia
tx: Tx with smaller meals more frequently, high-fiber foods, holding liquids when eating
______ hypersecretion of insulin in early stages of DM
Occult Diabetes Mellitus
What is the tx for a hypoglycemic pt? Give both conscious and unconscious pt
ask about hyoglycemia at every visit!!
conscious pt: 15-20 g of glucose is preferred tx. check BS again in 20 minutes and repeat if necessary
Unconscious Patient - IV glucose (20-50 mL of IV D50W), 1-mg IM or 3-mg IN glucagon kit
What is the recommendation for a DM pt who is about to exercise with a pre-exercise glucose is <100 mg/dL?
consider ingesting carbs prior to beginning exercise
DM pts are more prone to _____ which can worsen HTN. DM pts are also more prone to ______ (due to the osmotic effects of hyperglycemia) and increased _____
chronic kidney disease
intravascular volume expansion
arterial stiffness
_____ is as important as glycemic control to prevent DM complications! What is the target range?
BP control
< 130/80 mmHg - Especially if if 10-year ASCVD risk ≥ 15%
What are the ASCVD risk factors?
LDL-C ≥100 mg/dL
HTN
smoking
overweight/obese
(+) family history of premature ASCVD
What is the recommended tx for DM pts who BP > 120/80 mmHg?
Weight loss
Increased physical activity
DASH-style dietary pattern
Decreased sodium (<2300 mg/day)
Increased potassium intake
Increased fruit/vegetable intake (8-10 servings/day)
What is the recommended tx for DM pts who BP >130/80 mmHg? What do you need to monitor?
Lifestyle changes
Pharmacotherapy (Regimen including ACEI or ARB)
Monitor serum creatinine, eGFR, and potassium
When would you start BP meds on a pregnant pt? When would you reduce dose? What is the goal BP?
Start/adjust pharmacotherapy if BP is >140/90 mmHg
Reduce dose if BP <90/60 mmHg
Goal BP of 110-135/85 mmHg
Pregnancy-safe BP meds - labetalol, hydralazine, nifedipine, methyldopa
What is the lipid monitoring for a DM pt NOT on a statin? On a statin?
Not currently on a statin - lipid panel at DM dx, and at least every 5 years thereafter
Currently on a statin - lipid panel at the start of statin tx and “periodically” thereafter
aka ususally q6months when you check A1c
If pts have TG over _____ or HDL over ____ in men and ____ in women need to recommend lifestyle changes and ensure glycemic control is optimal
If pts have TG ≥ 150 or HDL ≤ 40 (men), HDL ≤ 50 (women)
If DM pts have fasting TG over ____ need to evaluate for secondary hypertriglyceridemia; consider medication to reduce _____ risk
If pts have fasting TG ≥ 500
need to start rx to reduce pancreatitis risk
What is the risk/benefit argument when it comes to DM and statin therapy? What should you consider adding on?
**Benefit of CV event risk reduction is thought to outweigh risk of DM
If pts do not respond to or cannot tolerate high-intensity statins - may consider statin + ezetimibe or statin + PCSK9 inhibitor
DM pts who can’t tolerate statins regardless of age the best alternative to statin therapy is ??????
bempedoic acid (Nexletol) or PCSK9 agents
Weight-loss medications may be considered in DM pts with a BMI _____
Bariatric sx can be considered in DM pts with a BMI ____ and/or with poorly controlled DM/comorbidities
BMI ≥ 27
BMI ≥ 30
What are some positive prognostic factors for a DM pts who is considering bariatric sx?
young, short DM duration, lower A1c, higher endogenous insulin
When should you screen for tobacco use in DM pts?
EVERY visit!!!
What are the 3 characteristics of a severe hyperglycemic state? all 3 are present in ____ and _____
Severe hyperglycemia (usually >250 mg/dL)
Volume depletion
Relative or total lack of insulin
DKA and hyperglycemic hyperosmolar state (HHS)
A pt in DKA, _____ is the typically major finding. What is the normal glucose range? What is the normal pH range? Is the dehydration greater or less in DKA?
Metabolic acidosis
Glucose - typically 250-600 mg/dL; rarely >800 mg/dL
pH - usually 6.8-7.3
less dehydration in DKA
Will there be ketones present in HHS? What is the typical glucose range? What is the typical pH range? Is the dehydration greater or less in DKA?
Ketones - little or no ketoacid accumulation
Glucose - typically >600 mg/dL; often >1000 mg/dL
pH - usually >7.30, with serum bicarbonate >20 mEq/L
dehydration is GREATER is HHS
What is the pathophys behind DKA? What 2 hormones in particular? What is the biggest trigger of DKA?
Relative or absolute insulin deficiency plus excessive counterregulatory hormones (glucagon, epinephrine, cortisol, growth hormone)
insulin deficiency and glucagon excess
Infections!!
During DKA, what is happening in terms of glucose? In terms of fats?
increased hepatic gluconeogenesis and glycogenolysis → hyperglycemia
increased release of free fatty acids → increased ketone body formation by liver
At physiologic pH, ketones exist as _____ and are neutralized by ______. What happens when the bicarb runs out?
ketoacids
bicarbonate
Depletion of bicarb → metabolic acidosis
Abdominal pain and tenderness frequently present
Often have a “fruity” or “acetone” smell to breath
1+ days of ↑ thirst with marked polyuria and polydipsia
Hypotension
Tachycardia
alert or drowsy in mild cases
severe: may be confused, lethargy or coma
What am I?
MC in T1DM or T2DM?
What type of breathing is associated?
DKA
classically in T1DM
Kussmaul respirations - deep, labored breathing pattern seen in severe metabolic acidosis, classically with DKA
Why is there elevated to normal potassium in DKA? Will sodium be decreased/normal/elevated? Bicarb? renal function?
normal or elevated (5-8 mEq/L), despite total-body K+ deficit
Due to intracellular → extracellular K+ shift with acidosi
sodium: decreased (125-135 mEq/L)
bicarb: decreased
Renal function - often see elevated BUN/creatinine, decreased eGFR
What 3 ketones are common to see in DKA? **Which one is the major one? Is urine or serum better?
acetone, acetoacetate, and β-hydroxybutyrate
β-hydroxybutyrate is manufactured 3x more than other ketones
Urine tests - primarily detect acetoacetate, sometimes acetone
Serum tests - can more reliably detect true ketone levels as they can sense the presence of β-hydroxybutyrate as well
urine tests will NOT pick up β-hydroxybutyrate which is the ketone that causes the most problems
What is the first step in DKA management? What do you do if hypernatremia occurs? ____ is associated with worse outcomes
Rapid infusion of 1 L/hr 0.9% normal saline solution (NS) for 1-2 hours
After ~2 L infused, decrease rate to 300-400 mL/hr
Change to 0.45% NS solution
Inadequate (<3-4 L in 8 hours)
How many liters is the typical DKA pt deficit? _____ increases a pt’s risk of respiratory distress and cerebral edema?
4-5 Liters
Excessive (>5 L in 8 hours)
DKA monitoring: should measure _____ every 1 hr and _____ every 4 hours for the first ____
FSBG
electrolytes/anion gap
24 hours
DKA management: _____ is given IMMEDIATELY following fluids. What should you do if no response? What do you need to be mindful of?
IV regular insulin based on Initial bolus of 0.1 U/kg, then 0.1 U/kg/hr by continuous IV infusion
Increase insulin by 2-3x if no response within 2-4 hours
If serum K+ is <3.3 meq/L - do not give insulin until potassium is corrected
adjust insulin to decrease glucose by about 75 mg/dL per hour
When serum glucose reaches 200 mg/dL, add dextrose-containing fluids
Goal to maintain serum glucose in the 150-250 mg/dL range
Reduces risk of cerebral edema
Continue IV insulin along with IV glucose to continue promoting resolution
of ketosis and acidosis
DKA management: Potassium will gradually ____ as acidosis resolves and ____ moves back into cells. What are the infusion recommendation?
drop
K+
Recommended to start infusion of 10 mEq/hr roughly 2-3 hours after starting tx, when:
Plasma K+ <5.0–5.2 mEq/L
ECG normal (no peaked T waves)
Urine flow and normal creatinine have been documented
If bicarbonate given or K+ <3.5 mEq/L - administer 40–80 mEq/hr
As part of DKA patient education, Ketone measurement when glucose is greater than ______
300mg
What is HHS (Hyperglycemic Hyperosmolar
State) due to ? What is the MC pt?
Relative insulin deficiency coupled with inadequate fluid intake. Lower counterregulatory hormones and free fatty acids than in DKA. Have some insulin present
Middle-aged or older patient with T2DM. Often goes on longer before tx and higher rates of morbidity
marked polyuria
may have polydipsia
typically have altered mental status - confusion, lethargy, coma
Hypotension and tachycardia due to volume depletion
What am I?
What is the serum glucose levels usually between?
HHS
typically 600-1200 mg/dL; may be even higher
What is the blood pH in HHS? What is potassium? Sodium? bicarb?
Blood pH - normal or minimally acidotic (>7.3)
Potassium - typically normal
Sodium - 135-145 mEq/L - can vary with osmolality
Serum bicarbonate - usually normal or minimally decreased
What is the renal function of a HHS patient? Serum osmolality?
prerenal azotemia
↑ BUN/creatinine (BUN often >100)
↓ eGFR
330-380 (often >350)
What is the first step in HHS management? How many liters?
Fluids - first step in management, Rapid infusion of 1-3 L 0.9% NS over the first 1-3 hours
typically have deficit of 6-10 L
What is the monitoring for a pt with HHS?
FSBG every 1 hour and renal function/electrolytes every 4 hours for the first 24 hours
What is the second step in HHS management?
What is the HHS management regarding potassium?
K often normal when they first get admitted but once insulin is given, will drop potassium levels
Recommended to start infusion of 10 mEq/hr. May consider starting with initial fluids if patient is normokalemic
Consider higher rates if K+ is low (<3.5 mEq/L)
Caution in patients with CKD - higher risk of hyperkalemia
What are the 3 microvascular complications of DM?
retinopathy
nephropathy
neuropathy
What are the 3 macrovascular complications of DM?
increased risk of stroke
increased risk of heart attack
peripheral vascular disease
______ leading cause of blindness in adult US pts! What is the initial stage called?
Diabetic retinopathy
Nonproliferative (“background”) retinopathy
What is proliferative retinopathy? What is the management?
involves growth of new capillaries and fibrous tissue within the retina and into the vitreous chamber. Small vessel disease → retinal hypoxia → release of VEGF
good BS and BP control
Photocoagulation of new vessels
Anti-VEGF intraocular injections
What increases your risk of diabetic retinopathy?
higher A1c
What is the initial manifestation of diabetic nephropathy? What test is used?
proteinuria
Spot urine albumin/creatinine ratio
(In-office urine dip - does not detect very early stages of albumin excretion)
When should Spot urine albumin/creatinine ratio be completed? How do you interpret the results? What is the most accurate test?
Preferably done in early AM on at least two occasions (Jensen prefers at least 1 time a year)
Normal - ratio of <30 mcg/mg; microalbuminuria - ratio of 30-300 mcg/mg;
macroalbuminuria - ratio of >300 mcg/mg
Urine 24-hr collection for protein
What is the management of diabetic nephropathy?
Good BS control!
low protein diet
Antihypertensive tx - preferably with an ACE or ARB
Antidiabetic tx - SGLT-2 inhibitor therapy and/or GLP-1 agonist therapy
Mineralocorticoid Receptor Antagonists (MRAs) - reduce proteinuria and CKD progression (eplerenone, spironolactone, finerone)
If diabetic nephropathy is not well managed, what could happen? Give some lab findings
nephrotic syndrome
Massive proteinuria
Edema
Hyperlipidemia
Hypoalbuminemia
_______ MC DM peripheral neuropathy. What does it present like? What is it due to?
Distal Symmetric Polyneuropathy
stocking-glove” distribution; generally appears first in feet
denervation of foot musculature and atrophy of the muscle
What is the tx for peripheral neuropathy?
good BS control!!
supportive footwear
avoiding foot ulcers
painful neuropathy may require pharm management (TCAs, gabapentin, duloxetine)
What is the gastroparesis tx? severe cases?
May be treated with metoclopramide (Reglan), erythromycin
Severe cases - botulinum toxin injection to pyloric sphincter, electrical stimulation
What is the tx for incomplete bladder emptying? What is the tx for orthostatic hypotension?
May be managed with medication (bethanechol), catheter decompression, surgery
compression stockings, elevating head of bed, arising slowly from sitting and supine positions
Severe - fludrocortisone, midodrine
To help manage CVD complications from DM ____ is recommended in individuals with >10% 10-year CHD risk
ASA 81mg qd
Why do DM patients tend to more frequent and severe infections? Which type specifically?
Hyperglycemia impairs phagocytosis and vascular disease impairs blood flow
fungi
______ if severe hypertriglyceridemia. What is the tx?
Eruptive cutaneous xanthomas
Yellow nontender papules with erythema; seen on extensor surfaces
Often diminish once triglycerides are controlled
_____ are brownish, rounded, painless atrophic macules in the pretibial area. What is the tx?
Pigmented pretibial papules/Diabetic dermopathy/Shin spots
no tx!
______ oval or irregular, well-demarcated plaques with glistening yellow surface; usually anterior legs or dorsal ankles. What is the tx? What type of DM pts?
Necrobiosis lipoidica diabeticorum
tx: Treated with topical steroids and improving glycemic control
Usually seen in insulin-dependent patients
