Glucose Flashcards
(117 cards)
1
Q
What is the difference in DM between dogs and cats?
A
Dogs = absolute insulin deficiency –> immune-mediated destruction of beta-cells (± pancreatitis ± genetic factors)
Cats = relatice insulin deficiency
2
Q
Name 5 secondary causes of DM
A
hypersomatotropism
HAC
exogenous glucocorticoids
diestrus
pregnancy
3
Q
What is glucotoxicity?
A
persistent hyperglycemia causes beta-cell damage
4
Q
What die Fletcher and DiFazio report about early insulin administration in dogs with DKA?
A
more rapid resolution of DK/DKA without an associated increase in complications
5
Q
What is the goald with insulin treatment?
A
glucose 150-250 mg/dl
6
Q
Name 2 causes of PU/PD in DM
A
- obligate diuresis due to osmotic diuresis
- medullary washout secondary to PU/PD
7
Q
When should continuous glucose monitoring be checked with blood glucocse?
A
- periodical checks
- unexpected readings
- glucose >500mg/dl or < 60mg/dl
8
Q
What dose of magnesium can be given if hypokalemia does not respond to supplementation?
A
1mEq/kg/d
9
Q
What causes hypokalemia in DKA?
A
- renal loss
- vomiting
- inappetence
10
Q
What causes hypophosphatemia when treating DKA?
A
- osmotic diuresis
- metabolic acidosis
- insulin therapy
- fluid therapy
supplementation: potassium phophate CRI 0.06-0.12mmol/kg/hr
11
Q
What is the downside of giving capromorelin to a patient with DM?
A
= ghrelin agonist –>
MOA: raises IGF1 levels –> may increase insulin resistance
12
Q
Why might glucose levels rise when giving a blood transfusion?
A
anticoagulat = CPDA = citrate phosphate dextrose adenine
13
Q
How are common are concurrent diseases in dogs and cats with DKA? What are the most common ones?
A
Dogs: 74%
Pancreatitis, HAC, bacterial UTI, neoplasia
Ctas: 93%
pancreatitis, bacterial + viral infections, neoplasia, hepatic lipidosis, cholangiohepatitis
14
Q
What are the 4 counterregulatory hormones of insulin?
A
glucagon
epinephrine
cortisol
Growth hormone
15
Q
Describe the pathomechanism of DKA development
A
Lack of inuslin causes decreased cellular glucose utilization –> cells become deficient but glucose levels in serum are rising –> osmotic diuresis –> dehydration + hypovolemia –> renal perfusion + glucose excretion decrease –> exacerbation of hyperglycemia –> when cellular metabolic needs cannot bemet anymore –> increase in counterregulatory hormones to mobilize alternative energy sources:
–> hepatic glycogenolysis
–> hepatic gluconeogenesis
–> lipolysis + decreased FFA storage
–> increased circulation of FFA –> oxidation in mitochondria via b-oxidation –> AcetylCoA –> usually goes into citrac acid cycle for ATP formation, BUT: in DKA Acetyl-CoA carriers in the citric acid cycle are reduced –> excess Acetyl-CoA –> oxidation –> ketone bodies:
- acetoacetate
- b-hydroxybutyrate
- acetone
16
Q
What causes metabolic acidosis in DKA?
A
b-hydroxybutyrate
acetoacetate
–> both moderately strong acids that dissociated significantly at phsiologic pH
17
Q
What are other important contributing factors apart from lack of insluin, that contribute to ketogenesis in DKA?
A
- increase in counterregulatory hormones (even glucagon despite detectable to normal levels of insulin)
- cytokine dysregulation
18
Q
Are there any predispositions in signalment for DKA?
A
one study: intact females overrepresented: 43%
19
Q
What is the diagnosis of DKA based on?
A
- compatible clinical signs
- persistent hyperglycemia and glucosuria
- ketonemia or ketonuria
- metabolic acidosis (based on serum bicarbonate)
20
Q
How common are the following findings in DKA in dogs?
- hyperglycemia
- Ketonuria
- Metabolic acidosis
- increased AG
- hyponatremia
- hypochloremia
- ihypocalcaemia
A
Hyperglycemia: 98-100%
Ketonuria: 94-100%
Metabolic acidosis: 93%
increased AG: 77%
hyponatremia > 50%
hypochloremia > 50%
ihypocalcaemia > 50%
21
Q
What concentration of ketones are associated with DKA in dogs and cats?
A
Dogs: >3.5 mmol/L
cats: >2.4 mmol/L
22
Q
What haematology findings may be present in DKA?
A
- normochromic, normocytic anaemia (50%)
- leukocytosis with left shift
- thrombocytosis (not in cats)
23
Q
What biochemistry findings may be present in DKA?
A
- raised ALP (up to 97%)
- raised ALT, AST, GGT, lipase, amylase (50% of dogs)
- azotaemia (cats > dogs)
24
Q
What causes electrolyte loss in DKA? Why might this not be evident on initial blood testing? In % of dogs can rapid declines in a) K+ and b) phosphorus be seen after IVFT and insulin therapy?
A
Hyperglycemia + hyperosmolality –> shifting of water, K+, phosphorus, Mg2+ from intra- to extracellularly –> osmotic diuresis causes significant water + electrolyte loss –>
- dehydration + hypovolemia
- total body K+, phosphorus, and Mg2+ depletion
This might be masked initially due to:
- decreased renal perfusion + excretion
- hypoinsulinemia
- acidosis (K+)
–> after IVFT + insulin rapid declines in
a) K+: 84%
b) phosphorus: 48% of dogs
25
Name 4 life-threatening consequences of severe hypokalemia + hypophosphatemia
1. muscle weakness
2. respiratory paralysis
3. conduction abnormalities
4. hemolysis
26
What causes hyponatremia in DKA?
1. electrolyte loss
2. dilutional due to hyperglycemia
3. ADH release due to decreased ECV
27
How (much) does hyperglycemia influence serum Na+?
For every increase in 100mg/kg of glucose Na+ drops by 1.6 mEq/L
--> effect is non-linear: mild hyperglycemia leads to smaller changes in Na+ than more severe hyperglycemia
28
How common id bacterial UTI in dogs with DKA? What is the most common isolate?
13% (87% have negative cultures)
most common isolte: E.Coli
29
What are the goals of DKA therapy?
1. restoring IV volume
2. restoring interstitial volume
3. management of electrolyte + acid-base derrangements
4. clearing the body of detectable ketones
5. decreasing blood glucose levels
6. management of concurrent diseases
30
How can fluid therapy alone decrease hyperglycemia in DKA?
* increased renal perfusion --> excretion
* decrease in production of counterregulatory hormones
31
What type of resuscitation fluid should be used in DKA?
balanced isotonic crystalloids containing bicarbonate precursors as puffers (lactate, acetate, gluconate) -->
* faster resolution of metabolic acidosis
* decreases incidence of hyperchloremia
32
What has hyperchloremia been associated with in DKA?
* increased time to DKA resolution
* increased risk of AKI
* increased hospitalization time
33
What seems to be an important underlying mechanism for the development of neurological signs with the treatment of DKA?
Previously worry about decreasing osmolaltiy too quickly --> cerebral edema
BUT recent evidence:
inadequate normalization of serum Na+ concentration with resolution of hyperglycemia --> neurologic complications
34
What is the aim for decreasing blood glucose levels with insulin in DKA?
* <250mg/dl +
* ≤ 50-75mg/dl/hr
35
How can insulin be administerd in DKA?
* regular insuline CRI: 2.2U/kg in 250l bag of 0.9% NaCl
* intermittent IM regular insulin: 0.2 U/kg followed by hourly injections at lower dosages depending on glucose drop (>75mg/dl: 0.05U/kg; 50-75mg/dl: 0.1 U/kg; <50mg/dl: 0.2 U/kg)
* lispro insulin
* insulin aspart
* IM regular insulin up to q6hr + glargine BID
36
What did Gallagher et al JVECC 2015 report when comparing regular insulin CRI to intermittent IM regular insulin + glargine BID?
IM regular insulin up to q6hr + glargine BID group had shorter time to biochemical resolution of DKA + shorter time to hospital discharge
37
When is bicarbonate therapy recommended in people with DKA? Why would be increasing the pH in DKA patients be beneficial?
pH <7.0 after 1hr of IVFT
acidemia can lead to a acidosis-induced insulin resistance
38
Name 3 negative effects of bicarbonate administration to treat metabolic acidosis in DKA
1. worsening hypokalemia
2. decreased tissue oxygen delivery
3. paradoxical intracellular acidosis
39
When can DKA patients be transitioned to long-term insulin therapy?
1. eating + drinking
2. resolution of ketonemia
40
What diet is re commended for dogs and cats with DKA/DM?
DKA: anything
DM:
dogs: high-fiber diet
cats: high-protein, carbohydrate restricted diet
41
What are reported survival rates for DKA in dogs and cats? What is the median hospitalization time? How common is recurrence of DKA?
Dogs: 52-81% (lower in dogs with HAC), MHT: 6d; recurrence: up to 17%
Cats: 61-100%; MHT: 3-7d; recurrence: up to 42%
42
What is associated with a decreased likelihood of survival in dogs and cats?
Dogs: HAC, ionized hypocalcemia, anaemia, more severe acidosis
cats: more severe azotemia, metabolic acidosis, hyperosmolality
43
What is the recommended treatment schedule for dogs and cats with DKA?
44
What are the criteria for HHS in dogs and cats?
1. Hyperglycemia > 600mg/dl
2. abscence of urinte ketones
3. serum osmolalit > 325 mOsm/kg (dogs) or > 350 mOsm/kg (cats)
45
What is a normal serum osmolality for dogs and cats? With what osmolality have neurological signs been documented in animals?
dogs: 302 mOsm/kg
Cats: 318 mOsm/kg
Neuo signs > 340 mOsm/kg
46
How many dogs with HHS had recent steroid administration?
18%
47
How can you calculate the osmolality and the effective osmolality?
serom osm (calc) = 2xNa + [BUN (mg/dl)/2.8 + glucose (mg/dl)/18]
effective osm = 2xNa + [glucose (mg/dl)/18]
48
How can you calculate the corrected sodium?
Na (corr) = na (meas) + 1.6 x [(measured glucose-100/)/100]
49
How common is HHS in diabetic dogs?
5%
50
What are the 3 contributing factors causing HHS?
1. Hormonal alteration [relative or absolute lack of insulin + increase in counterregulatory hormones in response to additional stressors (e.g. infection, diseases)]
2. reduction of GFR (due to hypovolemia + dehydration, reduced thrist response to rising ADH levels in people)
3. Concurrent disease
51
What is the pathophysiological difference between HHS and DKA?
In HHS lipolysis is inhibited by
1. hyperosmolar state
2. hepatic glucagon resistance
3. presence of small amounts of insulin
--> no FFA --> no ketone body production (via b-oxidation to Acetyl-CoA and then oxidation to ketone bodies)
52
What are the consequences of reduced insulin levels
elevated counterregulatory hormones (e.g. epinephrine, glucagon) in HHS?
* inhibition of muscular glucose uptake (epinephrine + glucagon)
* stimulationf hepatic glycogenolysis + gluconeogenesis (epinephrine + glucagon)
* inhbition of insulin activity (Cortisol + growth hormone)
* potentiation of the effects of glucagon + epinephrine (Cortisol + growth hormone)
* increased protein catabolism --> provides AA for hepatic gluconeogenesis
53
What correlates with the severity of neurological signs in people with HHS?
* elevated BUN levels
* acidemia
* elecated Na+
* osmolality
but NOT glucose concentration
54
Apart from the effects on glucose homeostasis, what are other pathological processes going on in a diabetic crisis?
* increase in proinflammatory cytokines (TNFa, ILs)
* increase in CRP
* increase in ROS
* increase in plasminogen activator inhibitor-1 (PAI-1)
55
Why can severe hypoglycemia only occur in the presence of a reduction in GFR?
Because here is no maximum rate of glucose loss via the kidney --> every glucose in excess of renal threshhold that is filtered and not reabsorbed will be excreted
56
Name 5 diseases that are throught to predispose a previously stable diabetic to a diabetic crisis
1. renal failure
2. CHF
3. infection
4. neoplasia
5. endocrinopathies
57
How many dogs with HHS had concurrent pancreatitis?
1/3 (in cats pancreatitis + heptic diseases is an uncommon diseases with HHS --> difference to DKA)
58
Why does CHF and renal failure predispose a diabetic patient to HHS?
renal failure: reduction in GFR, isosthenuria --> more diuresis
CHF:
* decreased GFR (decreased CO + renal perfusion)
* diuretic use
* thrid-space fluid loss
* b-blockers + diuretic alter carbohydrate metabolism
59
What are the most common biochemical abnormalities in cats with HHS?
* azotemia
* hyperphosphatemia
* elevated AST
* acidosis
* hyperlactatemia
* hypochloremia
60
Are dogs with HHS with or without ketosis more likely to be azotemic?
ketotic < nonketotic
61
What causes metabolic acidosis in dogs with HHS?
accumulation of uremic caids + hyperlactatemia
62
What has been associated with a poor outcome of HHS in dogs?
low pH
abnormal mental status
63
What is the main determinate of serum osmolality?
Na+
64
How is serum Na+ altered in HHS?
increase: due to renal free water loss
decrease:
* hyperglycemia-indued osmotic pull of water into the vasculature (dilutional)
DM in general - decrease due to:
* altered ADH metabolism
* insulin-potentiation of ADH induced acquaporin expression
* slower gastric emptying
65
How is serum K+ altered in HHS?
decrease:
* renal loss due to osmotic diuresis
* vomiting
* hyporexia/inappetence
increase:
* acidosis
* severe hyperosmolality
* insulin deficiency
* poor renal perfusion + decreased excretion
66
What are the main goals for management of HHS?
1. replacing fluid deficit
2. slowly reduce glucose levels
3. address electrolyte abnormalities
4. treat concurrent disease
67
What is important regarding the management of HHS?
slow reduction in glucose level! --> no more than 50-75mg/dl/hr
if glucose is dropped too rapidly --> cerebral edema
68
What fluid therapy (incl. stategy for fluid plan) is recommended for patients with HHS?
1. balanced crystalloids with higher Na+ content (e.g. normosol R, plasa-lyte 148)
2. 12-15% dehydration assumed --> replaced within 24-48hr
3. include urine losses as part of replacement volume (due to high losses via osmotic diuresis)
4. iof hypernatremic after sodium correction calc: addition of free water (enteral or IV hypotonic 0.45% - CAVE don't use D5W due to glucose content)
69
How does HHS differ from DKA regarding insulin therapy?
not as important for reversal of HHS because it's mainly due to hyperglycemia which can be improved with fluid therapy only due to improvement in GFR + correction of fluid deficit
Nonketotic HHS: insluin should not be given until hypovolemia has resolved, hydration has improved and glucose concentrations are no longer adequately declining (<50mg/dl) with appropriate fluid therapy only
Ketotic HHS: low dose insulin might be needed sooner, but correct electroylte derangements first!
--> if glucose is dropping by more than 50-75mg/dl/hr --> reduce insulin dose by 25-50% or add dextrose to IVFT
70
At what glucose level should dextrose be added into IVFT with insulin therapy for HHS?
<300mg/dl
71
Name 3 complications of HHS (treatment) that have been documented in people
1. Venous thromboembolism (common)
2. rhabdomyolysis (uncommon)
3. malignant hyperthermia-like events (rare)
72
What is the mortality rate of HHS in adults, children, cats and dogs?
Adults: 5-17%
children: up to 72%
cats: 64.7% (long-term survival (> 2m): 12%
dogs: 38%
73
Name 3 negative prognostic indicators in people with HHS?
* lower GCS
* higher plasma glucose
* mild acidosis
74
Discuss glucose homeostasis.
75
What are the 3 main sources of glucose in the body?
1. intestinal absorption
2. Glycogenolysis
3. Gluconeogenesis
76
What are nonhormonal mechanisms in glucose homeostasis?
1. Hypothalamus detects glucose concentrations --> adjusts feeding behavior + sympathetic output
2. SNS:
--> stimulates hepatic glycogenolysis even before hormonal responses fully engage
3. Autonomic nervous system:
input from other organ systems (GIT, brain, liver)
4. Skeletal muscle contractions:
--> stimulate GLUT4 translocation to the cell membrane independently of insulin
77
Name 3 general mechanisms for the development of hypogycemia
1. inadequate dietary intake
2. excessive glucose utilization
3. dysfunctional glycogenolyitc or gluconeogenic pathways or inadequate precursors
4. endocrine abnormalities
78
Why is inadequate dietary intake not enough to cause hypoglycemia in the adult patient? Why are neonates prone to hypoglycemia with inadequate nutritional glucose intake?
periods of fasting stimulate gluconeogenesis + glycogenolysis
Neonates:
1. incompletely developed glycogen stores
2. incomplete hepatic enzyme function
3. brain accounts for most of the basal metabolic rate
79
For what organ is glucose an obligate energy source and why?
Brain:
1. can only store minimal amounts of glycogen
2. cannot manufacture glucsoe
80
What defines the severity of neuroglycopenia?
degree, rate of decline and duration of hypoglycemia
81
What is a common consequence sequelae of prolonged neuroglycopenia?
can lead to permament brain injury + neurological signs --> blindness!
82
What causes clinical signs of hypoglycemia like pacing, restlessness, shaking and vocalizing?
activation of adrenergic system:
83
Why might patients with prolonged periods of hypoglycemia not show clinical signs?
= hypogylcemia unawareness --> chronic or recurrent hypoglycemia induces upregulation of cerebral glucose uptake --> decreases the brain's perception of peripheral hypoglycemia
84
How is hypoglycemia dianosed? When do clinical signs occur?
definition = glucose ≤ 60mg/dl
clinical signs often do not develop until < 50mg/dl
85
What is the Whipple's triad?
guideline for identifying hypoglymia --> 3 points:
1. clinical signs consistent with hypoglycemia
2. low blood glucose
3. improvement of signs with correction of hypoglycemia
86
When taking peripheral blood samples without sampling from a vein, what areas have been desribed and which one is the most accurate?
1.paw pad
2. MM
3. medial aspect of ear --> most accureate
87
What causes pseudohypoglycemia?
if serum is not seperated from RBCs + WBCs --> cells consume glucose via glycolysis --> artificial low glucose level in analysis
88
How do neurons take up glucose?
Insulin is not required for this!
Mainly faciliated diffusion via:
1. GLUT-1
2. GLUT-3
--> glucose concentration gradient (between arterial blood + intracellular) is important for maintaining gradient
89
What patients are predisposed to exogenous insulin overdose?
1. cats > dogs
2. obesity
3. cats receiving > 6 IU of insulin per injection
4. anorexic/hyporexic patients receiving insulin
5. patients who vomit after insulin injection
90
Does the severity of hypoglycemia depend on the amount and type of insulin given? Make a plan for restarting insulin after a period of iatrogenic hypoglycemia?
No
1. confirm insulin needs to be restared (hyperglycemia)
2. reduce dosgae by 25-50%
3. monitor grlucose regularly
4. check if there is an underlying disease the predisposed patient to hypoglycemia e.g. infection)
91
What is of most prognostic value in patients experiencing an exogenous insluin overdose?
response to therapy
--> cats that recovered showed significant improvement in neuro signs within 12hr
92
What might be done to diagnose insulinoma, if hypoglycemia is not initially present to take a sample for simulatenous insluin + glucose measurements?
* supervised fast
* multiple samples
93
Calculate the amendd insulin/glucose ratio. Why is this helpful?
AIGR = (insulinx100)/(plasma glucose -30)
... if plasma glucose < 30mg/dl assume denominator of 1
AIGR <30 suggetsted insulinoma, but not other causes of hypoglycemia can lead to a low ratio as well
94
What diagnostic imaging may be done when insulinoma is suspceted?
1. thoarcic radiographs to check for metastasis
2. AUS
3. CECT
4. MR scintigraphy
95
What treatment results in the longest survival times for insulinoma?
medical only: 196d
surgery only: 785d
combination of surgical excision (+ excision of metastasis) + medical management upon recurrence --> 1316d
96
How many patients with insulinoma have metastatic disease evident at the time of surgery?
50% (+ majority has occult metastasis)
97
Name 6 treatments for medical management of insulinoma and theit MOA
1. small, frequent meals with diet low in simple sugars
2. glucocorticoids (prednisone 0.5-1mg/kg PO divided in BID; or higher) --> increases glucose production
3. diazoxide (10mg/kg intitially, up to 60mg/kg divided q12hr) --> inhibits insulin secretion
4. streptozocin --> destroys pancreatic b-cells
5. somatostatin analogs --> suppressses insulin syntehsis + secretion
6. alloxan --> b-cell cytotoxin
7. toceranib (tyrosine kinase inhibitor) --> antiangiogenic + antiproliferative effects
98
What hormones do insulinomas express?
1. GH + GH receptor
2. insulin-like growth factor 1
3. insulin
99
What effect does toceranib have on the treatment of insulinoma?
Dogs that were surgically managed + then administered
toceranib after relapse survived longer than those that did not get
toceranib
--> 50% of the toceranib dogs surviving 357 days after relapse vs. 147 days for the non-toceranib dogs
100
What are the 3 stages of insulinoma and how does this affect prognosis?
Stage I: confined to pancreas --> 50% disease-free 14m postop, MST: 766d
Stage II: local lymph node metastasis --> MST 574d
Stage III: distant metastasis --> MST: 6m
101
What factors were predictive of disease-free interval + survival in dogs with insulinoma?
* tumor size
* TNM classification
* presence of necrosis
* biomarker Ki67 index
DFI only: presenve of nuclear atypia
102
How can tumors cause hypoglycemia?
What tumors have been reported to cause paraneoplastic hypoglycemia?
1. secretion of insulin or Insulin-like peptides
2. accelerated glucose consumption by tumor cells
3. failure of hepatic glycogenolysis or gluconeogenesis
Tumors: hepatomas, hepatocellular carcinomas, leiomyomas, leiomyosarcomas, + other carcniomas or adenocarcinomas (mammary, pulmonary, salivary, hepatocellular), lymphoma, oral melanoma, HSA
103
Name 4 drugs/toxins that cause hypoglycemia and their MOA
1. sulfonylurea durgs: chlopropamide, glipizide --> stimulate insulin secretion, enhance tissue sensitivity to insulin, decrease basal hepatic glucose production
2. xylitol --> b-cells insulin release
3. b-blockers --> interference with adrenergic counterregulatory mechanisms
4. oleander plant (unlcear)
104
Name 4 factors predisposing nursing animal to hypoglycemia
1. premature birth
2. debilitation of the bitch/queen at paturition
3. being the runt of the litter
4. diabetes in the bitch
105
Name 7 factors predisposing weaned animal to hypoglycemia
1. concurrent infection
2. vaccinations
3. vigorous exercise
4. GIT upset
5. poor nutrition
6. hypothermia
7. extended fast
106
Name 5 DD that must be considered in a hypoglycemic puppy/kitten
1. PSS
2. glycogen storage disease
3. sepsis
4. hepatic disease
5, coutnerregulatory hormone deficiency (e.g growth hormone deficiency)
107
Name 5 hormonal deficienceis that can lead to hypoglycemia
1. cortisol
2. glucagon
3. GH
4. thyroid hormone
5. catecholamines
108
Name 4 causes of excess glucose utilization
1. infection
2. extreme exercise
3. polycythemia or leukocytosis
4. pregnancy
109
What causes hypoglycemia in sepsis?
1. decreased intake
2. decreased hepatic function
3. non-insulin mediated increased consumption induced by inflammatory mediators (TNF) in macorphage-rich tissues like spleen, liver and lungs
4. increased anaerobic glycolysis due to hypotension or hypoxaemia
110
Name one specific parasitic disease (apart from sepsis) associated with hypoglycemia, where hypoglycemia is also a poor pronogistic indicator. What is the cause of hypoglycemia in this disease?
Canine babesiosis
causes: same as sepsis + consumption of glucose by parasites
causes of hypoglycemia in sepsis:
1. decreased intake
2. decreased hepatic glucose production
3. non-insulin mediated increased consumption induced by inflammatory cytokines (TNF) in macrophage-rich tissues like spleen, liver and lungs
4. increased anaerobic glycolysis secondary to hypotension or hypoxaemia
111
What causes exercise-induced hypoglycemia?
Esp. in hunting dogs
1. glycogen depletion due to increased endogenous glucose production (glycogenolysis, gluconeogenesis) in order to meet increased demand because of massive glucose utilization in muscle
112
How does polycythemia or leukocytosis induce hypoglycemia?
Secondary to:
* increased metabolism of glucose
* reduced plasma volume
--> primarily an artificial change and does not usually result in clinical signs
113
How may anaphylaxis cause hypoglycemia?
1. increased cellular utilization
2. decreased hepatic production or mobilization of glucose
3. translocation of bacteria across compromised GI
114
What can be used in the home-setting to treat hypoglycemia?
* Karo syrup
* pancake syrup
* honey
115
How can you reduce the risk of peripheral cetheter phlebitis with dextrose administration?
* lower dextrose concentration
* faster infusion rates of higher dextrose concentrations
* elective re-siting of IV infusions
* if dextrose >10% --> central line
116
If hypoglycemia is refractory to supplementation, what other therapy could you instigate? How is this associated with survival?
1. glucagon CRI: bolus of 50 ng/kg followed by CRI of 5-40ng/kg/min (choose lowest effecte level to maintain low normal euglycemia)
--> Non-survivors needed higher glucagon dosages
2. glucocorticoids
117
Name 11 causes of hypoglycemia
1. counterregulatory hormone deficiency
2. hepatic dysfunction
3. anaphylaxis
4. Hypocortisolism (HA)
5. neonates
6. sepsis
7. toxins (xylitol)
8. excercise-induced
9. paraneoplastic (lymphoma, hepatoma, hepatocellular carcinoma, oral melanoma)
10. insulinoma
11. iatrogenic overdose
