Diabetic Complications Flashcards
Hypoglycemia is plasma gluc < ____ mg/dL
50
Whipple triad
- low blood sugar
- presence of symptoms
- reversal of these symptoms when the blood sugar level is restored to normal.
Hypoglycemia effects on nervous system
Stim sympathoadrenal nervous system (adrenergic) -> sweating, palpitations, tremors, anxiety, hungry
Neuroglycopenia
LOW cerebral glucose -> confusion, difficulty with concentration, irritability, hallucinations, focal impairments (eg, hemiplegia), and, eventually, coma and death.
Repeat hypoglycemia episodes are super dangerous bc…
they will have less and less adrenergic symp and will eventually just go straight to a comatose state
Exercise and Pregnancy can cause _____
Hyper or Hypo -glycemia?
Hypoglycemia
drugs that can cause hypoglycemia
haloperidol
quinine
salicylates
sulfonamides
oral hypoglycemics (Sulfonylureas primarily)
insulin
isoniazid
methanol
methotrexate
tricyclic antidepressants
cytotoxic agents
fluoxetine
sertraline
trimethoprim
thiazide diuretics
ACE-I
tramadol
lithium
those with _____ syndrome are at higher risk of insulin-producing tumors of the pancreas -> hypoglycemia
MEN 1 (Multiple endocrine neoplasia type 1)
MCC of hypoglycemia in DM pts?
- injecting insulin and skipping a meal
- overdosing insulin
Qs to ask pt presenting with nocturnal hypoglycemia?
- taking drugs late at night after supper?
its usuallly a sulfonylurea
Early and late SS of hypoglycemia
- Early -> Neurogenic (adrenergic)
- Late -> Neuroglycopenic
Normally, eating a snack with ____ and ____ is enough to improve mild hypoglycemia
sugar and protein
(juice + PBJ sandwich)
liquid sugar incr blood gluc in 15 min
Dextrose Trmnt for hypoglycemic episodes
orally 4-20g, repeat every 15 min
IV 10-25g
Glucagon for hypoglycemia
1 mg ( 1 unit) IM/SC/IV
intranasal 0.3mg into 1 nostril
often used when there is no IV access for Dextrose
give _____ if pt overdoses on Sulfonylureas
Insulin Inhibitors
- Diazoxide: effect starts within 1 hour, lasting a maximum of 8 hours
- Octreotide: Used for sulfonylurea overdoses when more than 1-2 boluses of D50W are ineffective to control hypoglycemia
Prevention of Hypoglycemia
- Never take insulin or medications that decrease postprandial BS without food in front of you!
- If exercising >60 min, reduce last dose of fast acting insulin and eat a larger portion of carbohydrates
- If doing a long exercise, like running or biking for several hours, decrease basal insulin dose the night before and do #2.
GREEN SLIDE MUST KNOW
Eldery diabetics have _____ A1C % targets than adults. (Usually ___%)
higher or lower?
higher
8.5%
Causes of Hyperglycemia
- Reduction in physical activity
- Incr in carbohydrates in diet without ability to increase Med or inadequate changes
- Physical stress of illness, trauma, or surgery
- Infx: UTI, Pneumonia, flu or Covid
- Corticosteroids
- Missed diabetic medications
Pt admitted for hypoglycemia has a sugar goal of ____
140-180
refer to sliding scale insulin
Pathophysiology of Hyperglycemia
Hyperglycemia results in sorbitol deposits into sensory and autonomic nerves resulting in axonal degeneration and segmental demyelination.
It also causes microvascular disease in blood vessels by wall thickening of small arterioles and capillaries. This occurs in the nerves, kidney, retina, heart and brain.
These wall changes promote atherosclerosis in these vesselsà ischemic changes in these organs
*Vit D deficiency is linked to increase in coronary artery calcifications in DM type I pts
____ deficiency is linked to increase in coronary artery calcifications in DM type I pts
Vit D
SS of Hyperglycemia
Common -> Fatigue, Hunger, Thirst, Frequent urination Blurry Vision
Reallyyyyy bad -> Nausea and vomiting, Abdominal pain, Fast breathing Confusion, Coma
DKA
insulin deficiency + hyperglycemia -> ketoacidosis (fat breakdown -> ketones for energy).
too many ketones -> acidic blood and urine
often triggered by infx or stopping insulin
ketoacidosis occurs in which organ?
liver
What are the 3 ketones?
acetone
beta- hydroxybutyrate
hydroxy acid
____ ketone is what causes fruity breath in DKA
Acetone
Why do pts in DKA exhibit kussmaul breathing?
trying to compensate for metabolic acidosis by breathing off CO2 (hyperventilating)
why does DKA cause nausea and vomitting?
Ketones, specifically beta-hydroxybutyrate cause nausea and vomiting, which worsen the dehydration
How does DKA affect K+ and H+ diffusion?
in DKA, is there more K+ in the cells or serum? What will K+ labs show?
Insulin is needed for K+ to enter cells. More K+ in the serum than cells. Water follows K+, cells shrivel, results in hypovolemia and you pee out our volume. K+ labs are NORM despite there being LOW K+ in the cells! dont be fooled
Causes of DKA in Type 1 DM
Causes of DKA in Type 2 DM
Infx
Steroids
SS of DKA
Initiallly -> Polydipsia, Polyuria, **Fatigue, General Weakness
As ketone levels rise -> N/V + Diffuse abd pain + Anorexia +/- rapid wt loss
Kussmaul breathing + sweet acetone breath
Dehydrated -> dry skin, etc
VS -> tachycardic and tachypneic, hypotensive, hypothermic or fever
Eventually -> abd pain, confusion, coma
DDx of DKA
Acute pancreatitis
Appendicitis
UTI
Hypophosphatemia
All the causes of metabolic acidosis: MUDPILES
WU for DKA
- ABG
- CMP
- CBC
- Blood Beta-Hydroxybutyrate levels
- UA
DKA WU
CMP Serum K+ calcuation
Subtract 1.6mEq/L for actual serum K+ for each 100mg/dL over 100mg of glucose
Hypokalemia can cause which arrhythias?
premature ventricular complexes
atrial fibrillation
atrial flutter
supraventricular tachycardia
torsade de pointes
ventricular tachycardia
ventricular fibrillation
Anion GAP calculation
What calculation can you do to determine risk for coma or cause of coma?
serum osmolatiry
2(Na + K) + BUN/3 + glucose/18
If >290 = DKA
>330 = coma
Additional blood tests for DKA
Imaging orders for DKA
CXR
Brain MRI or CT if in a coma/altered mental status– looking for cerebral edema
DKA ECG changes
Peaked T wave changes
usu due to hypokalemia -> more K+ in serum/interstitium than in RBC.
DKA Trmnt checklist
- Correct fluid loss with IVF
- Correct hyperglycemia with insulin(potassium)
- Correct electrolyte disturbances, particularly potassium loss
- Correct acid-base balance, the above may do this, on its own
- Tx any infection found
Begin treatment in ER and then admit to ICU for 24-48 hours depending upon severity
DKA fluid correction
Lactated Ringers
1-3 L in 1st Hr
1 L in 2nd Hr
1 L in following 2 Hrs
1 L q 4hrs, depending on degree of dehydration and BP
DKA Fluids
When Glucose falls to 180-200 (provider dependent), IVF is replaced with _____
D5 1/2NS
E- replacement for DKA
When you begin your IVF, you must consider Potassium replacement.
If:
Low or normal (<5.5mEq/L), add 20-40mEq of KCL or KPO4 to IV bag. So each liter they will get 20-40 mEq of Potassium
DKA
Begin insulin after ____ Hr of IVF
1
initial insulin dose is a continuous IV insulin infusion using an infusion pump, if available, at a rate of 0.1 U/kg/h.
Once glucose hits 180-200, insulin infusion dose is cut in half
Optimal rate of blood glucose fall is 100 points an hour, any faster will result in rebound ketosis due to stimulation of counter regulatory hormones.
*do not start insulin if potassium is <3.3, replace potassium first
DKA
Pt is on IVF and CMP K+ <3.3
Can we start insulin?
NO
replace K+ first
DKA
don’t give insulin without ____
K+
K+ dosages when giving Insulin
While infusing insulin, we stop adding potassium to the IV bags and hang a little bag of it by itself.
if >6mEg/L, wait
4.5-6, give 10 mEq/hr 3-4.5, double (20mEq/hr)
Monitor hourly
DKA
IVF to correct Acid-Base imbalance
Usually corrects on its own as fluids and insulin correct dehydration and electrolyte imbalances.
If high volume of fluids results in worsening acidosis, or patient is septic, sodium bicarbonate can be infused usually 100-150mL of 1.4% every half hour as needed.
DKA Discharge
DKA Trmnt Complications
- Cerbral Edema (associated with ongoing hyponatremia and correlated with giving bicarbonate)
- Cardiac Dysrhythmia
- Pulmonary Edema
- Myocardial Injury
- Hypoglycemia
- Hypokalemia
Who gets it?
Hypersomolar Hyperglycemia State
Type II DM
ET: Infx, CVA, MI
SS: hyperglycemia, hyperosmolarity, and dehydration without ketoacidosis
DKA vs HHS
- Type II DM get HHS
- Type I DM get DKA
- There is some insulin in HHS. Enough to suppress lipolysis and ktogenesis, but not enough to prevent hyperglycemia
*
Once blood glucose hits 180, it supersaturates the renal tubules with glucose and they can hold no more. The kidneys then no longer reabsorb glucose and it passes through into the urine. This creates an osmotic diuresis, so water and electrolytes flow out through the urine as well.
At approx. blood glucose level of 210, a dipstick will have enough glucose to be positive
HHS Pathophysiology
Low insulin -> high glucose -> hypertonicity -> diuresis -> hyperosmolarity of plasma triggers ADH release -> incr water reabsorption thru collecting ducts of kidneys -> Dehydration and THIRSTY -> hypovolemia -> HypoTN stim RAAS -> Oliguria (pee little) results in less Gluc being peed out -> coma
Meds that can cause high gluc and inhibit insulin or cause dehydration
1 SS of HHS in Type II DM
Change in level of consciousness (drowsiness, lethargy, delirium, coma)
Other: seizures, vision changes, sensory probs, hemiparesis
HHS PE
Focus on evaluating hydration status, s/s of infx, and mental status
VS: hypotension, tachycardia, fever, tachypnea
PE: dry mucous membranes, decreased skin turgor, prolonged cap refill, anhidrosis, decreased urine output, lethargic, ill looking, sunken eyes, weak pulse.
HHS PE
HHS Dx labs
Plasma glucose >600 mg/dL
Serum osmolality of >320 mOsm/kg, Normal from 280 to 290 mOsm/kg.
Profound dehydration, up to an average of 9 L Serum pH greater than 7.30
Bicarbonate concentration greater than 15 mEq/L Small ketonuria and absent-to-low ketonemia
HHS WU
ABG, CMP, CBC
Osm = (2 × Na) + (glucose/18) + (BUN/2.8)
Normal serum osmolality ranges from 280 to 290 mOsm/kg.
Usually Patient is not acidotic because there are no ketone bodies being utilized, no there should not be an anion gap.
Na- (HCO3 + Cl) =12 +/- 4
BUN will be elevated due dehydration
CBC may have elevated WBC and left shift due to infx
UA – elevated sp gravity due to high osmolarity of blood. Elevated glucose, also looking for signs of infx
CXR – looking for infx
Head CT - exclude hemorrhagic strokes, subdural hematoma, subarachnoid bleeding, intracranial abscesses, and intracranial masses.
ECG – MI can cause it. The height of the T waves may point to a potassium derangement. The duration of the QT interval may be abnormal as a consequence of calcium abnormalities.
LP – for suspected meningitis
HHS Trmnt
- ABC
- Fluid Resuscitation
- Insulin continous infusion
- Monitor BS
~~~
```Which DM complication can leave you blind?
Diabetic Retinopathy
Type I Diabetics need eye exam within ____ yrs
5
SS of diabetic retinopathy
Initially -> asymp
Late -> floaters, blurred vision, distortion, progressive visual acuity loss
Diabetic Retinopathy Trmnt
- A1C goal 6-7%
- lower BP
- Early laser trmnt decr risk of vision loss
What causes Diabetic Neuropathy
Sugar in nerves breaksdown nerve structures -> abnormal AP
Always symmetrical
MC complication of DM (Type I & II)
Diabetic Neuropathy
Are burning finger tips a (-) or (+) sensory symp?
(+) burning pain
(-) cant feel
____ is the 1st clinical sign of diabetic neuropathy (diabetic symmetrical sensorimotor polyneuropathy)
Decr or loss of Vibratory and pinprick sensation over the toes
WU for Diabetic Neuropathy
Electrophysiologic testing: EMG
MRI if possible radiculopathy
A1c, urinalysis looking for protein since they will often also have nephropathy
Pain control for Diabetic Neuropathy
Neurontin
Lyrica (edema risk)
Tricyclic antidepressants-amitriptyline SNRIs: Duloxetine, venlafaxine
Capsaicin Topical cream for mild symptoms
What supplements can help glycemic control and reduce paresthesias?
B Vit & Zinc
Charcot Arthropathy
Cant feel feet -> repeat trauma -> progressive destruction of bone and soft tissues at wt bearing joints
Charcot Arthropathy can lead to what structural changes of the feet?
Clubfoot due to fracture and collapse
Rocker-bottom foot due to collapse and plantar arch inversion
Charcot Arthropathy WU
CBC, looking at WBC ESR
CMP
A1c
Phosphorus, Calcium, PTH, alk phosàlooking for Paget’s, CA B12, folateàalcoholics
RPR/fluorescent treponemal antibodiesàsyphilis
XR with weight bearing if possible
Bone scan if osteomyelitis suspected
Charcot Arthropathy Trmnt
REFERALLLLLLLL to foot and ankle specialist
Tx fractures – mean time is 18.5 weeks, compared to 6 weeks for normal bone
Tx ulcers with wound therapy and antibiotics Special footwear
Total heal time is 1-2 years
Surgery required in 25%
Diabetic Gastroparesis Tx
Constipation predominant:
MiraLax (polyethylene glycol 3350)
Ø metoclopramide (Reglan)
Ø cisapride (Propulsid)
Diarrhea predominant:
Ø Loperamide (lmodium), diphenoxylate (Lomotil)
Autonomic Neuropathy
Orthostatic HypoTN
Low norepi levels
they dont vasoconstrict well
Tx: venoconstriction (alpha 2 adrenergent agonist Miododrine), SNRI/SSRI, compression stockings, incr water and salt, stand up slowly
Autonomic Dysfn Trmnt
Urinary Dysfn Trmnt
Mild Dysfn?
Spastic Bladder?
Detrusor Areflexia?
Refractory situations?
Diabetic Nephropathy Dx
- HIGH BP
-
Persistent albuminuria (>300 mg/d or >200 μg/min) that is confirmed on at least 2 occasions 3-6 months apart
With: -
Progressive decline in the glomerular filtration rate (GFR<60) or
the presence of diabetic retinopathy and/or having type 1 diabetes greater than or equal to 10yrs in duration
Diabetic Nephropathy Pathophys
Diabetic with Foamy urine is a sign of _____
Diabetic Nephropathy
also have proteinuria
Type I DM pt has nephropathy. They likely also have…
Microvascular Dz (Retinopathy, Neuropathy)
Diabetic Nephropathy WU
Microalbumin/creatinine ratio
Persistent albuminuria (>300 mg/d or >200 μg/min) that is confirmed on at least 2 occasions 3-6 months apart
A consistent decline in the glomerular filtration rate (GFR)
Elevated blood pressure
CMP – look at BUN/Creat and GFR
Renal US – confirms no obstructive process, also will show normal or increased size which rules out other types of nephropathies which result in atrophy
Nephropathy Diet Restrictions
- Protein (goal 0.5-1g/kg/day)
- Phosphorus and K+ (phosphate binders)
- Salt Restriction (5-6g/day)
Nephrotoxic Drugs to avoid in Nephropathy
1st line HTN med for nephropathy
ACE/ARB (renal protective)
lifestyle and OTC trmnt for HTN in pts with diabetic nephropathy
Salt reduction
Vit D Supplements (kidneys help produce Vit D)
vitamin D supplementation: Evaluate anyone with stage 3 kidney dz(GFR30-59) for vit d def and PTH. Treatment of vitamin D def. may reduce proteinuria in patients with diabetic nephropathy.
3 drug classes that are great for Glucose control in diabetic pts
Direct DM Nephropathy Trmnts
- Kerendia
- Avosentan
- Ueno
End-Stage Renal Disease (GFR 10-15mL) Trmnt Options
- nothing -> die
- Peritoneal Dialysis
- Hemodialysis
- Renal Transplant
There is a dose-response relationship b/w blood glucose levels and the development of _____
an arrhythmia
Atrial Fibrillation
