14.9 (14.2) Endocrine and metabolic complications from advanced cancer Flashcards
What is the most common life threatening metabolic disorder from cancer?
Hypercalcemia
Malignancy related hypercalcemia
List 4 etiologies and list for each:
i) frequency
ii) main mechanism
iii) 1 tumour related
TABLE 14.9.1:
- Local osteolytic (bone mets):
i) 20%
ii) bone resorption from increased osteoclast activation by local factors (RANKL, cytokines, chemokines, prostaglandin) from bone mets
iii) breast cancer, MM, prostate (cancer with bone Mets) - Ectopic production of PTHrP (ie Humoral
Malignant Hypercalcemia)
i) 80%
ii) PTHrP
–> (1) Bone: increased RANKL expression –> osteoclast activation -> bone resorption
—> (2) Renal: decreased renal clearance of calcium
iii) Solid tumors = SCC of any organ, renal, bladder, breast, endometrial, ovarian - Ectopic production of Calcitriol (active form of Vit D) production
i) <1%
ii)Enhanced calcium absorption from gut
iii) lymphomas - Ectopic production of PTH
i) <1%
ii) Bone resorption, decreased renal clearance of calcium, enhanced absorption from gut due to PTH
iii) none listed - very rare?
List 2 ways in which osteoclasts cause hypercalcemia?*
- Secrete hydrogen and chloride ions causing dissolution of hydroxyapatite
- Produce lytic proteases which dissolve organic bone matrix
What is the role of RANKL?
What is the role of osteoprotegrin (OPG)?
How does malignancy affect RANKL expression?
List two cancers in which OPG quantity is decreased.
RANKL = osteoclast activating factor that stimulates the RANK membrane receptor on osteoclast precursors -> differentiation into osteoclasts
OPG = “decoy receptor” for RANKL that competitively inhibits RANK binding
RANKL/RANK/OPG equilibrium is disrupted by cytokines, chemokines and prostaglandins –> loss of homeostatsis b/w osteoclast resorption, osteoblast bone formation.
Tumour cells directly produce RANKL or stimulate bone stromal cells to produce RANKL.
Also, calcitriol, PTHrP, IL-1, IL-6 enhance RANKL expression, diminish OPG expression.
OPG is decreased in myeloma and prostate ca
- Define humoral hypercalcemia of malignancy
- List 2 lab features that makes it biochemically similar to primary hyperparathyroidism (explain mechanism)
- Which biochemical test can differentiate between the two conditions? List 2 other biochemical differences*
- Does PTHrP explain all biochemical findings in humoral hypercalcemia of malignancy?
- Humoral hypercalcemia is due to ectopic production of PTHrP
- i) Hypercalcemia (RANKL - bone resorption + decrease renal clearance)
ii) Hypo PO4 (renal wasting)
3.
PTH
- low in humoral malignant hypercalcemia
- elevated in primary hyperparathyroidism
Calcium absorption and calcitriol levels are low in humoral hypercalcemia because unlike PTH, PTHrP does not promote renal hydroxylation of vit D3.
- NO - other factors (cytokines) likely at play, even in absence of bone metastases
- In which tissues is PTH expresssed?
- In which tissues is PTHrP expressed?
** May not be very important to know?
- PTH only expressed in parathyroid glands
- PTHrP expressed in many tissues (breast, parathyroid, fetal liver, brain, cancer)
What types of tumors produce PTHrP?
List 2 organs affected by PTHrp
Solid tumors
Bone: increased osteoclastic bone resorption
Renal:
Decrease calcium clearance + increase PO4 clearance
List two cancers that result in hypercalcemia through increased production of calcitriol (active product of Vit D)
How does increased Calcitriol cause Hypercalcemia?
How is management of this form of hypercalcemia different than others?
Hodgkins, non-Hodgkins lymphoma, Human T-cell lymphotrophic virus (HTLV) type 1 leukemia/lymphoma (ATLL)
increased gut absorption of calcium (not seen in usual hypercalcemia of malignancy)
need to have low dietary calcium intake
What five cancers are most commonly associated with hypercalcemia?
breast
lung
myeloma
renal
squamous cell carcinomas of any organ
Most patients with hypercalcemia of malignancy have disseminated disease.
- What is the approx 1 year mortality rate for patients with hypercalcemia of malignancy?
- Median survival?
- 75% die within 1 year
- Median survival is estimated at 1-4 months
List 2 GU, 2 GI, and 2 cardiac, and 2 neurological clinical features of hypercalcemia
Table 14.9.2
GU - polyuria, polydipsia, dehydration, stones
GI - constipation, anorexia, weight loss, nausea, vomiting, ileus
Neuro - fatigue, lethary, confusion, myopathy, hyporeflexia, seizures, psychosis, coma
Cardiac - bradycardia, atrial arrhythmia, ventricular arrhythmia, prolonged P-R interval, reduced QT interval, wide t waves
FS: moans, bones, groans, stones
- What is the order in which symptoms of hypercalcemia may progress?
- How is the severity of symptoms correlated with degree of serum calcium elevation?
- i) malaise/lethargy
ii) thirst, nausea, abdo pain, constipation
iii) drowsiness, confusion
iv) cardiological features - Not correlated (Apparently!)
What is the formula for corrected calcium?
corrected calcium = measured calcium + ([40 - serum albumin (g/L)] x 0.02)
List 3 management approach to treat hypercalcemia
Name 4 calcium lowering agents
1. IV fluids (rehydration) mild: 3-4 L/day oral fluids symptomatic/severe: IVF, 4-6 L of NS in first 24 hrs pall patients: 1-3 L in first 24 hrs Avoid immobility Watch for fluid overload Loop diuretic for volume overload, NOT as calcium lowering therapy NO role for low-calcium diet 2. Stop drugs promoting hypercalcemia (thiazide diuretics, vitamins A, D, and calcium supplements) 3. Start calcium lowering agents: bisphosphonates are 1st line, all else is 2nd line: - corticosteroids (if hematologic malignancies, breast Ca flare from endocrine Rx) - calcitonin (reduces osteoclast resorption, increases calciuresis; s/e: nausea, hypersensitivity rxn) - denosumab (2nd line, for refractory hyperCa2+ despite bisphos Rx, als reduced skeletal events in bone mets, myeloma). Monoclonal Ab to RANKL. Schedule: 120 mg days 1, 8, 15, 29 (seems very frequent?!**) then q4 weeks. Watch for nausea. - calcimimetics: molecules that potentiate effect of calcium on PTH secretion. Cinaclet approved for secondary hyperPTH + parathyroid CA, may be 2nd line Ca2+ lowering agent TBD (anecdotal) Others FROM 5th edition: Plicamycin Oral phosphates gallium nitrate
- What is the mechanism of action of bisphosphonates?
- In which type of malignancy-related hypercalcemia might bisphosphonate therapy fail?
- How often may bisphosphonate therapy be repeated after effective treatment?
- Reduce bone resorption by binding hydroxyapatite crystals with high affinity, inhibiting their breakdown (inhibit osteoclast activity) + promoting osteoclast apoptosis
- Humoral Hypercalcemia of malignancy without bone mets
(Bisphosphonates do NOT alter PTHrP lelves, renal calcium reabsorption, RANKL, or OPG levels)
- In absence of tumour directed Rx, hyperCa2+ will recurr.
Re-check Calcium levels q3-4 weeks, repeat bisphosphonate if appropriate.
- What is the dosing for pamidronate? zoledronic acid?
- List 2 benefits of ZA over pamidronate
- How are they adjusted in renal failure? What is an alternative?
- List 3 side effects of bisphosphonate therapy
- Pamidronate 30-90 mg IV depending on serum calcium) at rate of 20 mg/hour
ZA 4mg IV over 15 minutes
- ZA corrects hypercalcemia faster and for longer than pamidronate
- No dose adjustment in mild to mod renal failure
Avoid in severe renal failure (Ibandronic acid approved for use if CrCL <30) - Hypocalcemia
(esp in patients with suppressed PTH)
Renal toxicity
(esp if dehydrated, CKD, nephrotoxic drugs)
Osteonecrosis of the jaw
(if prolonged use, old age, recent dental extractions)
List 3 types of cancers that cause ectopic ACTH production
lung cancer (SCLC, bronchial carcinoids) - 50%
islet tumor of pancreas - 16%
thymic carcinoids - 10%
FS:
Adrenocorticotropic hormone
Usually made in anterior pit gland
Works on adrenal glands to produce cortisol
How common are ectopic ACTH secreting (EAS) tumours? Paraneoplastic Cushing’s syndrome?
May not be important to know
ACTH secreting non-endocrine tumours are not uncommon BUT clinically overt Cushing’s syndrome is RARE.
EAS only accounts for 5-15% of Cushing’s syndrome (and cancer is usually occult at presentation) - that’s why clinical DDx important but biochemical overlap makes this difficult.
List six features of Cushings syndrome
(** = more specific to Cushing’s)
- **proximal muscle weakness/atrophy
- edema
- HTN
- mental changes
- glucose intolerance
- central weight gain/truncal obesity (** abnormal distribution -temporal, supraclavicular)
- easy bruising
- moon facies
- cutaneous striae (**large violaceous striae > 1 cm)
- hypokalemic metabolic alkalosis (severe cases)
- peripheral muscle wasting
- **reduced linear growth with weight gain in a child
~~~
FS:
Moon facies
Truncal obesity
HTN
Glucose intolerance
Easy bruising
Stretch marks
Proximal muscle weakness
List three first line tests to diagnose Cushings syndrome
Need 2/3 for diagnosis:
elevated 24h urinary free cortisol
elevated late evening salivary cortisol
failure of cortisol suppression in overnight low dose dex test (1mg at midnight and test at 8am)
A patient has an elevate ACTH, elevated 24 hour urinary cortisol and a late night salivary cortisiol, What are the two broad etologies for this?
How to distinguish between the 2 etiologies
Pituitary Adenoma: ACTH-dependent Cushing’s syndrome
Ectopic ACTH secretion (EAS) by tumor (lung, pancreas, thymic)
—-
If high dose dex (8 mg) does not suppress 8am cortisol (and ACTH remains high) - likely ectopic
(However, 50% of EAS tumours suppress with high dose dex so may require other testing - CRH stim test, venous sampling ACTH, pituitary MRI, CT chest/abdo, functional PET/CT etc)
In addition to anti-cancer treatment directed at EAS tumour, list 4 treatments for Cushing’s syndrome aimed at inhibition of steroid synthesis.*
- Ketoconazole
- Metyrapone
- Mitotane
- Somatostatin analogues
- Etomidate
What are the two types of malignancy associated with siadh?
Name two non cancer causes
sclc
carcinoid tumors (type of neuroendocrine)
secondary mets to lung or brain
Other causes:
- pulmonary infection
- meds
FS: Syndrome of inappropriate antidiuretic hormone ADH release
List 3 medications that may trigger SIADH
- antidepressants (SSRI’s, TCA’s)
- Lorazepam
- Carbamazepine
- Phenothiazines (e.g. prochlorperazine)
- Cytotoxic agents (cylcophosphamide, vincristine)
FS: anti-SIADH
Anti seizure - carbamazepine
Anti iiiouch - opioids
Anti anxiety - Ativan
Anti depression - SSRI
Anti hurling - haldol
Define mild, moderate, severe hyponatremia and the corresponding clinical symptoms
TABLE 14.9.3
- Mild (130-135): nausea, concentration deficits
- Moderate (125-129): nausea, headache, confusion
- Severe (<125): vomiting, cardioresp distress, seizures, coma
List 4 essential criteria to diagnose SIADH
- Plasma hypo-osmolality and plasma hypoNa (plasma osmolality <275mOsm/kg and Na<135) in the presence of:
- normal plasma/extracellular volume
- concentrated urine (Uosm >100mOsm/kg)
- High urinary sodium (UNa > 30 on normal salt/water intake)
AND exclude hypothyroidism, hypoadrenalism, diuretics
A patient presents with severe hyponatremia.
1. What is the imminent risk (specific organ)
2. What is the initial management?
- Regardless of how low Na is or whether acute/chronic, with severe symptoms there is an imminent risk of cerebral edema.
- Initial management = 3% hypertonic saline in critical care setting until 5 mmol/L rise (but no more than 10 mmol/L rise in first 24 hours).
If symptoms improve with first 5 mmol/L rise, can d/c HTS and adopt cause-specific treatment.
**Note this aggressive approach may not be ideal for EOL patients -depends on prognosis/GOC etc.
A patient is diagnosed with tumor associated SIADH that is chronic in nature.
What is your treatment approach (name 3)
What is important to consider with this treatment in pall care?
fluid restriction <500-750 mL/day
Oral salt tabs (sodium chloride)
stop offending meds
In palliative care fluid restriction is not desirable as it is unpleasant for patients and onerous for caregivers
?Not important to know**
Other non-standard treatments: tetracycline analogues - cause nephrogenic diabetes insipidus AND
vasopressin receptor antagonists
Non-islet cell tumors produce hypoglycemia through what major mechanism? *
List 3 characteristics of non-islet cell tumours*
through production of insulin like growth factors
Usually large, located in retroperitoneum or thorax. and histiologically are mesenchymal (sarcomas, mesothelioma etc)
List the 2 major approaches to treatment of secretory endocrine tumours causing hypoglycemia.
- CURATIVE RESECTION
(often not possible in non-islet cell tumours + metastatic insulinoma) - If no surgery, then MAINTAIN EUGLYCEMIA (by targeting tumour OR glucose regulation)
Options to target tumour:
- debulking surgery, arterial embolization of mets to palliate hypoglycemia
- targeted chemo
Name 4 endocrine tumors. List a treatment for each one
TABLE 14.9.4:
VIP-oma - octreotide, glucocorticoids, K and HCO3 during attack (6th ed: surgery, SSA, chemo)
Glucagonoma - octreotide, oral hypoglycemics, prophylactic anticoagulation (6th ed: chemo, surgergy)
insulinoma - IV glucose, frequent feeding, glucagon, diazoxide, octreotide, surgical debulking, chemo
gastrinoma (Zollinger-Ellison) - gastrectomy, PPI, H2 receptor antagonist, octreotide
somatostatinoma - chemo, surgery
FS: VIP-GIG (tx Octreotide)
*SSA = somatostatin analogues - have antisecretory and antiproliferative effect (treat symptoms from excess hormone secretion)
Name 4 secretory endocrine tumours and for each list:
i) 1 clinical feature
ii) common anatomical site
iii) % likelihood of being malignant
- Insulinoma
i) neuroglycopenia
ii) pancreas beta cells
iii) 10% malignant - Gastrinoma (Zollinger-Ellison)
i) peptic ulceration
ii) duodenum >pancreas
iii) >50% malignant - VIPoma
i) watery diarrhea, hypokalemia
ii) pancreas
iii) >50% malignant - Glucagonoma
i) DM, CHF, cachexia, migratory necrolytic erythema
ii) pancreas
iii) >70% - Somatostatinoma
i) DM, diarrhea, cholelithiasis
ii) pancreas > duodenum/jejunum
iii) >70%
What is the origin of carcinoid tumours? List 2 areas in the body where they can occur.
- Arise from serotonin producing cells
- Principally GI TRACT and LUNGS
Occasionally, pancreas, thymus, gonads
List three types of tumors associated with MEN1*
parathyroid
pituitary tumor
pancreatic islet cell tumor
List two types of tumors associated with MEN2a and MEN2b*
medullary thyroid ca
pheochromocytoma (adrenal)
List 3 features of carcinoid syndrome
diarrhea asthma/bronchospasm flushing pellagra (niacin deficiency B3) endomyocardial fibrosis right sided CHF from pulmonary valve stenosis and tricusp regurg
List 2 investigations to diagnose carcinoid syndrome
urinary excretion of 5-HIAA (breakdown of serotonin)*
platelet 5HT levels
somatostatin receptor scintigraphy (Octreotide scan)*
pet*
List three therapies for carcinoid syndrome
- curative surgery where possible OR palliative debulking to delay/reduce carcinoid syndrome
- hepatic artery embolization of liver metastases (helps with carcinoid symptoms)
- somatostatin analogues* (1st line to inhibit tumour products)
- Chemotherapy, alpha-interferon, targeted agents (mTOR, TKI’s) all 2nd line
- Cardiac surgery for valve replacement (depending on prognosis)
- Beta agonists for wheezing and codeine/loperamide for diarrhea
Others from 5th edition:
metoclopramide
cyproheptadine
Catecholamine secreting tumours arise from which 2 locations.
- adrenal medulla (pheochromocytoma)
- Extra-adrenal neural crest -derived tissues
(paraganglioma)
Which 3 hormones do pheochromocytomas secrete
Commonly EPINEPHRINE and NOREPINEPHRINE
But occasionally significant DOPAMINE
List four symptoms of an active pheochromocytoma
htn anxiety* tremor* palpitations* sweating* flushing* headache GI disturbance polyuria
FS: like panic attack
List 3 intervention + 2 med options for malignant pheochromocytoma
- Palliative surgical debulking if possible
- Radiolabelled iodine 131-MIBG
- Chemo
- If surgery/chemo not options, then palliative treatment with alpha and beta adrenergic receptor blockade
(i.e. start alpha blocker such as doxazosin, gradually titrate until symptoms palliated, then follow with beta blockade (bisoprolol, metoprolol) if needed for tachycardia)
List 2 scenarios in which is it is critical to establish effective ALPHA BLOCKADE in the treatment of pheochromocytoma.
- Prior to surgery/chemo to prevent CATECHOLAMINE CRISIS
- Prior to starting BETA blockade due to risk of triggering FATAL HYPERTENSIVE CRISIS secondary to unopposed alpha-adrenoreceptor stimulation
Adrenocorticol carcinoma (ACC) are ultra-rare. They are often large >10 cm on presentation and cause symptoms from mass effect, BUT 50% of tumours are also secretory. *
Which hormone do they commonly secrete?
List 3 treatments for ACCs.
- Hypercortisolism most common (aldoesterone, androgens less common)
i) surgical resection/palliative debulking
ii) mitotane (adrenolytic drug)
- has major impact on steroid biosynthesis so have to start replacement hydrocortisone
iii) chemotherapy
- Which cells does medullary thyroid carcinoma arise from?
- What hormone do these cells secrete? List 2 symptoms caused by this?
- List 3 treatments for Medullary thyroid carcinoma.*
- parafollicular C-cells of the thyroid
- Calcitonin - can cause diarrhea and flushing
i) Total thyroidectomy and lymph node dissection if needed - but 50% will still have elevated calcitonin
ii) Mild symptoms may respond to codeine and loperamide but if severe:
local debulking
hepatic arterial embolization
SSA (somatostatin analogues)
iii) If metastatic/recurrent disease, TKI’s are 1st line after surgery
Gynacomastia results from elevation of estrogen/androgen ratio.*
List 2 contributing meds and 2 underlying tumour types
List 3 treatments for gynecomastia. List 2 indications for treatment.
- Meds:
chemo (alkylating, vinca alakloids)
antiemetics (maxeran, phenothiazines)
antiandrogens
gonadorelin analogues
Estrogen/gonadotropin secreting tumours:
testicular (leydig, sertoli)
adrenocorticol
hepatocellular
HCG secreting tumours (NSCLC, testes, hepatoma, pancreatic islet cell)
- Persistent pain, cosmetic concerns
- stop culprit med or treat tumour
- estrogen receptor modulator (tamoxifen)
- danazol
- breast reduction surgery
- low dose radiotherapy
List four possible manifestations of gonadotropin secreting tumors*
precocious puberty in children*
secondary amenorrhea in women*
gynacomastia in men
hyperthyroidism
(Secrete FSH/LH)
Prolactin secretion from a tumor can cause what finding? How is it treated (name 1 med)
lactation
dopaminergic agonist bromocriptine
List 2-4 endocrine complications from cranial radiation
growth hormone deficiency*
hyperprolactinemia
gonadotropin deficiency*
secondary hypogonadism
thyroid dysfunction*
List five cause for renal failure in cancer patients (box 14.2.2)
infiltration by tumor
fluid depletion
electrolyte imbalance -> uric acid (TLS), hypercalcemia, paraprotein (myeloma), amyloid (myeloma), lysozyme (acute myelomonocytic leukemia), mucoprotein (pancretic ca), nephogenic DI (leiomyosarcoma)
urinary tract obstruction
iatrogenic (chemo, xrt)
paraneoplastic (membraneous glomerulonephritis, minimal change glomerulonephritis, membranorpoliferative glomerulonephritis, thrombotic microangiopathy)
pre-exisiting CRF
FS:
Pre-renal -
Dehydration
pre-exisiting CRF
Renal -
Iatrogenic -> nephrotoxic
Paraneoplastic -> glomerulonephritis
Post-renal
Invading tumor causing obstruction
List four possible paraneoplastic endocrine abnormalities that can arise from cancer*
non-islet cell tumor hypoglycemia
carcinoid syndrome
gonadrotropin secretion
hypothalamic-pituitary adrenal dysfunction
List 3 iatrogenic causes of anterior pituitary failure in cancer/palliative patients
List 3 tumour-related causes*
1.
Intracranial radiation
Intracranial surgery
Long-term opioids (affect GnRH leading to LH deficiency)
- Pituitary adenomas/carcinomas
- Mets from breast, lung, renal. gastric
- Tumours in the hypothalamus
What is the first line drug for the management of ectopic ACTH secreting tumor?
ketoconazole 200mg PO TID - NV, HA, pruritic rash, liver failure
(Blocks production of cortisol in adrenal gland)
List four causes for adrenal dysfunction in cancer patients
1. bilateral mets (tho hypoadrenalism rare - would need to replace 80% adrenal tissues) 2. infection (imunocompromised) 3. hemorrhage 4. surgery 5. drugs that impact CYP enzymes (ketoconazole) 6. sterioid use
FS
Vascular : hemorrhage
Infection
Neoplastic
Degenerative
Iatrogenic: steroid, surgery
A diagnosis of hyperinsulinaemic hypoglycemia (i.e. as found in insulinomas) is suggested by clinical symptoms that satisfy Whipple’s triad - list it’s 3 components.*
How is the diagnosis confirmed biochemically?
*
- symptoms compatible with hypoglycemia
- low plasma glucose concentration
- Symptoms relieved by eating and restoration of euglycemia
BIochemically, after a prolonged fast, there is inappropriately high insulin concentrations at time of symptomatic hypoglycemia
Define acute vs. chronic hyponatremia
How does symptom severity relate to this?
Acute if present for <48 hrs, chronic if >48 hrs
Acute/faster rate of fall in sodium associated with more severe symptoms
(vs. chronic, in which brain cells able to compensate against cerebral edema by secreting potassium/intracellular solutes)
List 4 potential cancer related causes for hypo or hyperthyroidism
surgery
radiotherapy
systemic anti-cancer therapy
euthyroid sick syndrome from advanced malignancy
HCG secreting tumour (due to structural similarities between hCG and TSH)
Define secondary adrenal insufficiency.
What is the most common cause?
What dose/duration of systemic corticosteroid puts patients at most risk for adrenal suppression?
Describe how you would taper corticosteroids where adrenal suppression is likely.
- Inadequate production of ACTH at level of pituitary gland
- Long term synthetic corticosteroid use due to negative feedback on HPA axis
- If taking supraphysiological doses of systemic corticosteroids (7.5 mg/day or oral prednisolone) for 3 weeks or more (can happen earlier too)
- Slowly, by 1-2 mg of prednisolone per week once physiological doses are reached, to allow adrenal recovery
List 3 clinical manifestations of hypoadrenalism.
What is standard replacement therapy
- profound weakness
- GI upset
- hypotension
- psychiatric manifestations
- Addisonian crisis (rarely)
Standard replacement therapy:
Hydrocortisone 20-25 mg daily in divided doses
Fludrocortisone 0.05-0.15 mg daily
Patients will primary or secondary adrenal insufficiency require additional corticosteriod doses during physiological stress
List 4 causes of pyrexia in advanced cancer
TABLE 14.9.5:
- infection
- neoplasm (paraneoplastic or CNS mets; e.g. leukemia, lymphoma, liver mets)
- chemo/immunotherapy
- drugs
(Abx, anticonvulsants, bisphos) - radiation
(pneumonitis, pericarditis, cystitis) - other non-infectious causes (adrenal crisis, VTE, CTD)
- infection and neoplasm most common causes
- neoplasm accounts for 10% FUO
- pyrogenic cytokines –> prostaglandin –> hypothalamus –> thermal homeostasis
How do you diagnose neoplastic pyrexia?
List 3 treaments for neoplastic pyrexia
- No reliable clinical features or tests to discriminate between infective and non-infective causes of pyrexia.
Diagnosis of exclusion after work up of reversible causes. If none, diagnosis of neoplastic pyrexia should be made to avoid endless infective screens/repeat Abx
- sponging
icepacks
fans
antipyretics (paracetamol, NSAIDS, steroids)
- List 3 causes of hyperglycemia in cancer patients
- Pre-existing diabetes (independent risk factor for cancer)
- Cancer-related treatments (steroids, immune check point inhibitors due to autoimmune effects on insulin secretion, TKI’s causing insulin resistance)
- Tumour-related effects
- anorexia-cachexia associated gluconeogenesis, impaired glucose tolerance, and insulin resistance
- pancreatic cancer
1 List 3 aims of diabetes management in advanced cancer
- What is the target blood glucose range recommended for patients in the last year of life
- In T2DM, list 3 changes you may need to make to diabetes management as cancer progresses (appetite/ weight decrease)
- How to manage T1DM
- Prevent/treat symptoms of hyperglycemia
Avoid hypoglycemia
Avoid diabetic emergencies such as DKA (type 1) and HHS
- 6-15 mmol/L
- i) Stop hypoglycemia inducing meds (sulphonylureas, insulin)
ii) reassess tolerance/safety of meds (ie. metformin - GI side effects, reduce in renal failure)
iii) short acting repaglinide within 30 min of meals if oral intake variable
iv) T1DM - may need to reduce insulin if poor intake, renal function but will cotinue to need basal insulin until death
When should corticosteroid induced hyperglycemia be treated? How is it diagnosed/monitored? How is it treated?
List 2 important considerations for managing hyperglycemia with enteral feeding
- BG >15 and prolonged course of corticosteroid is planned
BG levels rise 2-3 hours after morning steroid dose, returns to baseline 12 hours later. So check CBG before evening meal.
Short acting sulphonylurea or insulin in morning reduces risk of overnight hypoglycemia (reduce when tapering steroid)
Enteral feeding:
1. Consider diabetic specialist consult
2. Review carb content of feed with RD
3. Metformin is only diabetic tablet in liquid form
4. Type of insulin depends on duration/frequency of feed
List 4 cancer-treatement related causes of osteoporosis
How can this be assessed?
List 4 treatments
- Glucocorticoids
- Chemo (i.e. cisplatin)
- above cause renal loss of calcium, magnesium, and phosphate - Premenopausal women treated for breast/ovarian cancer
- Men with prostate cancer on androgen inhibition
Assess:
Early BMD and fracture risk calculation
Treatments (dependes on age, pre/post menopause, fracture risk):
calcium + vitamin D supplementation
bisphosphonates
denosumab
HRT
