Diabetic Crises Flashcards
describe the pathogenesis of DKA
without insulin,
-do not undergo glycolysis or glycogenesis
-hormone sensitive lipase not inhibited: fats broken down to free fatty acids, which leave the lipid depot and enter circulation, travel to liver, and via carnitine shuttle are brought into the liver to make acetyl-coA, eventually normally used to make energy
-but not glycolysis = no oxaloacetate = cannot make energy from fatty acids so body makes ketones instead (acetoacetate first, then BHB and a small amount of acetone)
-ketones will either be excreted in urine or the rest will go to other tissues to be used to make energy
describe the ppt version of pathogenesis of DKA
- absolute or relative deficit of insulin:
-insulin normally: stimulates glycolysis, glycogenesis, and inhibits gluconeogenesis and glycogenolysis
-without insulin, blood glucose increases
-insulin also normally inhibits hormone sensitive lipase and CPT (which helps with fatty acids uptake) so without insulin, fats are mobilized and start to increase ketone production
- rise in counter-regulatory (stress) hormones: increase glucose level
-epinephrine and glucagon: inhibit insulin-mediated glucose uptake in muscle and stimulate hepatic glycogenolysis and gluconeogenesis
-cortisol and growth hormone: inhibit insulin activity and potentiate the effects of glucagon and epinephrine
-increase protein catabolism, which impairs insulin activity and provides amino acids for gluconeogenesis
- stimulation of effects of HSL
-insulin or lack of is the MAIN regulator of ketogenesis (inhibiting or activating lipolysis)
-release of HSL: stimulates lipolysis and inhibits lipid synthesis, resulting in a large quantity of FFAs
-increased activity of CPT-1 increases FFA transport
-large supple of fatty acyl CoA plus deficiency in oxaloacetate (from glycolysis) overwhelm citric acid cycle capacity and increase ketone production
describe acetoacetate and BHB
- strong acids!
- AcAc and BHB usually produced 1:1
-in DKA, amount of BHB rises (>3:1) due to highly reduced state of mitochondria - fully dissociate at physiologic pH
- [H+] released exceeds buffering capacity, resulting in acidemia - once ketone production exceeds clearance and utilization, there is a rapid rise of ketone concentration
- fraction that is not reabsorbed and instead excreted through urine promotes osmotic diuresis
-decline in GFR (as from hypovolemia, dehydration) further inhibits renal clearance - negatively charged ketoacids are excreted with electrolytes, leading to electrolyte abnormalities
describe renal handling of glucose
- filtered glucose directly dependent on glucose concentration and GFR
- 90% of filtered glucose is absorbed in the proximal tubule via SGLT2
-secondary active transport - tubular transport maximum is limited
- SGLT2 blockers reduce glucose absorption, resulting in glucosuria
-induce solute diuresis and improve glycemia
describe SGLT2 inhibitors and how they contribute to eDKA
- block the reabsorption of glucose from the proximal tubule, leading to enhanced glucose excretion
- but these also increase renal reabsorption of ketone bodies
-which contributes to ketosis despite euglycemia - may inhibit beta cells, leading to increased lipolysis
-adds to pool of FFA available for ketone production - stimulate pancreatic alpha cells to release glucagon
-glucagon:low insulin ratio favors gluconeogenesis, glycogenolysis, and FFA metabolism
describe predisposing factors for cats for eDKA
mostly unknown (new to use!)
-new DM diagnosis
-1-2 weeks on a SGLT2 inhibitor
describe hyperglycemic hyperosmolar syndrome
- severe hyperglycemia: >600mg/dL
- serum osmolality >350 mOsm/kg
- minimal or absent ketones:
-circulating insulin inhibits HSL
-hepatic glucagon resistance
-combinations of HHS and DKA DO occur - predisposing factors: same as for DKA
-especially conditions predisposing to decreased GFR (CKD, cardiac dysfunction/pump failure)
describe pathogenesis of HHS
- hyperglycemia induces diuresis
- leads to dehydration/hypovolemia
- ultimately DECREASED GFR (key to development of this syndrome)
- resulting in severe hyperglycemia and hyperosmolality
- CYCLE!!!!
describe the hyperosmolality of HHS
- associated with marked hyperglycemia and hypernatremia (due to free water loss)
- neurologic signs if serum osmolality >340 mOsm/kg
-normal: 290-310 mOsm/kg
-effective osmolality = 2(Na+) + (glucose/18)
-AKA, glucose and sodium are most important in determining osmolality of a patient!
describe history and client complains of DKA, eDKA, and HHS
DKA:
1. known or new diabetic
2. PU/PD
3. dramatic weight loss
4. lethargy, weakness
5. mental dullness
6. anorexia, hyporexia
7. VOMITING
8. +/- signs of concurrent disease
9. occurs rapidly
eDKA:
1. known diabetic CAT on a SGLT2i, usually 1-2 weeks after initiation of SGLT2i
2. PU/PD
3. weight loss
4. lethargy, mental dullness
5. hyporexia/anorexia
6. vomting
HHS:
1. known or new diabetic
2. PU/PD
3. +/- weight loss
4. lethargy, weakiness
5. overt neurologic signs, esp when osm >340 mosm/kg
6. HYPOREXIA
7. vomtiing
8. +/- concurrent disease, esp renal dysfunction or heart disease
9. occurs over many days
describe the reasons for common physiologic findings associated with DM
- PU/PD: osmotic diuresis
- polyphagia: decreased glucose in satiety center
- weight loss: fat mobilization
- vomiting: CRTZ activation due to ketones or hyperosmolality
- signs of underlying disorder: pancreatitis, gastroenteritis
describe physical exam of DKA versus HHS
consistent with DM usually +/-
DKA:
1. moderate dehydration
2. mental depression
3. thin BCS
4. +/- icterus, hepatomegaly
5. +/- ketone odor
HHS:
1. severe dehydraiton
2. mental depression, obtundation, stupor
3. overt neuro abnormalities: ataxia, abnormal PLRs, seizures
4. +/- seizures, gallops, arrhythmia
5. +/- uremic odor
describe initial diagnostics for these patients
- ideal start:
-CBC, chem, UA - +/- imaging
- MINIMUM: big 4
-PCV/TS, azostick, glucose
-measuring glucose: biochemical analyzer is best, handhelds may be inaccurate (glucose too high to read so know the meter’s upper limit! lipemia also complicates) - measure ketones on ALL SICK DIABETICS
-urine dipstick: urine ketones or serum ketones
-ketone meter
describe BG, ketone, metabolic acidosis, and osmolality criteria for DKA, eDKA, and HHS
DKA:
-BG: greater than normal
-serum/urine ketones: positive
-metabolic acidosis: yes, ketones; can have lactate and uremia
-total caclulated osmolality not usually greater than 350 mg/dl
eDKA:
BG: normal to mild increase
serum/urine ketones: positive
metabolic acidosis: yes
total calculated osmolality: not usually >350mg/dL
HHS:
-BG: >600mg/dL
-serum/urine ketones: negative to small
-metabolci acidosis: yes, usually lactate and uremic acids
-total calculated osmolality usually >350mg/dL
describe the complete diagnostic evaluation for a sick diabetic patient
- CBC, chem, UA WITH CULTURE
- imaging
- endocrine testing as needed.indicated: thyroid, adrenal
what are common stressors that initiate DM crises
- infection
- pancreatitis
- hepatic lipidosis/cholangiohepatitis
- IBD
- CRF/CHF
- other endocrine disorders
etc.
describe clin path findings of sick diabetics
- hemoconcentration or anemia
- inflammatory/stress leukogram
- increased liver enzyme activities
- increased bilirubin
- lipemia, hypercholesterolemia (DKA)
- azotemia
- electrolyte abnormalities
but vary with concurrent disease processes
describe potassium abnormalities of sick diabetics
total body K+ is generally LOW, blood K+ usually decreases with treatment
if the effect is to decrease K+
-osmotic diuresis, glucosuria, ketonuria
-ketoacid excretion: electroneutrality
-insulin admin: activates Na/K ATPase, inhibits potassium efflux, and increases sensitivity to intracellular sodium
-renal dysfunction
-aldosterone secretion: hypvolemia
if effect is to increase K+
-acidemia
-hyperosmolality
-lack of insulin
-renal dysfunction
-these patients are in a whole body K+ deficit
-signs of hypokalemia: generalized muscle weakness, cervical ventroflexion (cats), hypoventilation if severe
describe hypomagnesemia and hypophosphatemia of sick diabetics
- changes similar to potassium
- expected to decline with insulin admin
-transported into cells via Na/K ATPase
-utilized for ATP production - decrease correlates with decline in blood glucose and hydrogen ions
- hypophosphatemia: severe deficit causes hemolysis
- hypomagnesemia:
-refractory hypokalemia
-weakness, ataxia
-arrhythmias
-seizures/muscle fasciculations
-may cause insulin resistance
describe how Na+ is influenced by hyperglycemia
- normal or elevated sodium + hyperglycemia reflects free water loss
- measured sodium is low (pseudohyponatremia)
-hyperglycemia/hyperosmolality
-hypertriglyceridemia - calculate a corrected sodium to better assess water loss
how to manage the happy but not acidotic ketotic patient?
- if small amount of ketones but still eating and drinking without vomiting, start as a standard diabetic:
-insulin (long acting)
-diet change
-etc - monitor for increasing ketones and clinical signs
describe the goals of therapy for sick diabetics
- FLUID AND ELECTROLYTE BALANCE
-start with balanced, isotonic replacement fluid
-volume resuscitation if needed (fluid bolus for hypovolemia)
-glucose, pH, and ketones will start to improve with fluids alone! dilution and improved GFR = urine excretion
-calculate dehydration and replace as needed, maintenance (40-60ml/kg/day), ongoing losses
-WATCH OUT FOR HHS PATIENTS WITH HEART FAILURE - insulin treatment
- symptomatic and supportive care:
-vomiting, nausea, etc, - find and treat concurrent disease
- consider referral! need 24/7 care!!
describe electrolyte therapy for sick diabetics
- monitor electrolytes at least q12hr
-the lower they are, the more frequent to monitor - EXPECT them to drop as soon as insulin is started
-esp for DKA patients
-may need to increase lyte supplementation rate if they are barely normal when insulin is started - anticipate need to intensively supplement until not ketotic and usually eating
- potassium:
-supplement with KCl or K-phos until no longer ketotic and eating
-starting point
–option 1: based on serum K+ concentration with maximum of 0.5 mEq/kg.hr
–option 2: can also start as 0.1-0.5mEq/kg/hr; higher rate for lower potassium concentration
-if using both KCl and K-phos, must add potassium rate provided by both
-provide 1/4 to 1/3 of potassium as K phos and the rest as KCl - magnesium:
-magnesium sulfate: 0.75-1mEq/kg/24 hr CRI - sodium:
-calculate corrected sodium
-hyponatremia will usually resolve with normalization of glycemia
-decrease SLOWLY if truly hypernatremia (max 0.5-1mEq/L/hr), slowly progressive - bicarbonate therapy:
-rarely needed
-consider only if:
–pH <7.1 or <8mmol/L
–no improvement after routine fluid therapy
–AND clinical for acidemia: unresponsive hypotension, seizures
-bicarb therapy is NOT innocuous: paradoxic CNS acidosis, worsening hypokalemia
when should insulin be started for a sick diabetic?
- DKA/eDKA:
-after shock/hypovolemia are resolved
-hypokalemia, hypoMg, and hypophos should be resolved: minimally at low end of ref range - HHS:
-after shock/hypovolemia are resolved
-once glucose stops decreasing with appropriate (large) volume of fluids (resuscitation, rehydration, ongoing losses): often once glucose is readable on glucometer - why not start immediately?
-can cause hypovolemia or shock
-glucose holds water in vascular space
-if glucose drops rapidly, water moves out of vascular spaces
-will reduce electrolyte concentrations, can be life threatening
-could cause cerebral edema in HHS: due to rapidly decreasing osmolality
-is NOT essential to resolution of HHS
