Endocrinology Flashcards
Differentiate between macrovascular and microvascular complications with diabetes
Macrovascular - medium and large size blood vessels involved - CAD, MI, stroke, PAD Microvascular - involve small capillaries - retinopathy, nephropathy, neuropathy
Discuss the stages of diabetic retinopathy
Non-proliferative
- asymptomatic but could have impaired vision due to macular edema
- progressive blood vessel change including microaneurysm, hemorrhage, hard exudate
Pre-proliferative
- macular edema
- venous shunts and possible bleeding
- intra-retinal microvascular abnormalities
Proliferative
- neovascularization (abnormal BV growth) and fibrous scarring
- blindness due to vitreous hemorrhage or retinal detachment
Discuss the presentation and management of diabetic retinopathy
Presentation - asymptomatic - blurry vision - darkening or distorted vision due to macular edema - cotton wool spots - exudates Management - follow with ophthalmologist - glycemic control - control HTN and lipids
Discuss the stages of diabetic nephropathy
- nephrotic syndrome Stage 1 - hyperfiltration (increased GFR) where kidney may increase in size Stage 2 - microalbuminuria due to damage of glomeruli - ACR 2-20 male or 3-28 in female Stage 3 - increased albumin excretion (macroalbuminemia), rising creatinine and increased BP - ACR >20 male or >28 female Stage 4 - GFR <75 with proteinuria Stage 5 - end stage renal disease, GFR <10
Discuss the management of diabetic nephropathy
- glycemic control
- blood pressure control
- ACEi or ARB to reduce albuminemia
Discuss the presentation of different types of diabetic neuropathy
Peripheral Sensory Neuropathy
- Neuropathic pain, numbness, paresthesia
- decreased tactile sensation (glove and stocking)
Motor Neuropathy
- muscle weakness
- reversible cranial palsy
Autonomic Neuropathy
- alternating constipation and diarrhea due to gastroperesis
- urinary retention
- erectile dysfunction
Discuss the presentation, investigations and management for diabetic foot ulcer/cellulitis
Presentation
- infected ulcer (erythema, warmth, swelling, pain) or pus
- necrotizing if soft tissue gas, skin discoloration or foul odor
Investigation
- wound swab
- CBC, blood glucose, ESR/CRP
- blood culture
Management
- Surgical
- debridement and cleaning
- revascularization
- osteomyelitis then amputation
- Wound care
- relieve pressure on ulcer
- wound cleaning and dressing
- Glycemic Control
- Antibiotic
- Mild: Keflex
- Moderate: Septra plus Amox-Clav or Clindamycin
- Moderate with deep tissue: IV Pip-Tazo, Meropenem, Moxifloxacin, Flagyl + CeftriaxoneDiscuss classification of infection and risk for osteomyelitis for diabetic foot ulcer
Classification
- Infected if >=2 of purulence, erythema, pain, warmth, swelling
- Mild if erythema extends <=2cm around ulcer
- Moderate: erythema extends >2cm around ulcer or involvement of deep tissue
- Severe: systemic toxicity or instability
Risks for Osteomyelitis
- Large ulcer
- deep ulcer, probing to bone
- visualization of bone
- ESR >70
- MRI to r/o
Discuss the pathophysiology, benefits, risks and dosing of biguanides
Pathophysiology - increase sensitivity of the cell to insulin Benefit - A1c lowering of 1-1.5% - low risk of hypoglycemia - improved cardiovascular risk Risks - contraindicated with eGFR <30 (increase risk of lactic acidosis) - GI side effects
Discuss the pathophysiology, benefits, risks and dosing of incretins
Pathophysiology - secreted in the gut and result in increased insulin secretion from the pancreas - glucagon like peptide-1 - glucose dependent insulinotrophic peptide Benefit - increase satiety and decrease gastric emptying which reduces weight gain - increase insulin secretion Benefits - A1c lowering of 1% - significant weight loss - low risk of hypoglycemia - some cardiovascular benefit Risks - GI side effects - subcutaneous injection required - rare cause of pancreatitis - increase parafollicular hyperplasia
Discuss the pathophysiology, benefits, risks and dosing of DDP-IV inhibitors
Pathophysiology - amplify incretin pathway by inhibiting breakdown of endogenous GLP and GIP Benefits - A1c lowering of 0.7% - low risk of hypoglycemia - improve post-prandial control - GI side effects
Discuss the pathophysiology, benefits, risks and dosing of SGL2-inhibitors
Pathophysiology
- block glucose transport in proximal renal tubule leading to urinary exretion
Benefits
- glycosuria:
- negative caloric balance and weight loss
- decrease A1c
- increase uric acid release
- natriuresis
- decrease blood pressure resulting in decrease arteriolar stiffness
- decrease plasma volume resulting in decreased myocardial stretch
- increase tubulo-glomerulo fedback and afferent arteriole constriction
Risks
- increase risk of UTI
- osmotic diuresis leading to hypotension
- ketoacidosis in euglycemic individual
Discuss the pathophysiology, benefits, risks and dosing of sulfonylurea
Pathophsyiology - bind to sulfonylurea receptor inhibiting efflux of K -> depolarization and increase in Ca entry into cell -> increase insulin release Benefits - A1c lowering of 0.8% - rapid glucose lowering Risks - may cause hypoglycemia - weight gain
Discuss the pathophysiology, benefits, risks and dosing of meglitinide
Pathophysiology - same as sulfonylurea as is a secretague Benefit - A1c lowering of 0.7% - rapid glucose lowering with lower risk of hypoglycemia due to shorter half-life - safe with renal impairment Risks - weight gain - hypoglycemia - interaction with plavix
Discuss the pathophysiology, benefits, risks and dosing of acarbose-glucosidase inhibitor
Pathophysiology - inhibit intestinal enzymes alpha-glucosidase and pancreatic alpha-amylase resulting in reduced digestion of carbohydrates Benefits - A1c lowering of 0.6% - rare hypoglycemia - GI side effects
Discuss the pathophysiology, benefits, risks and dosing of thiazolidinediones
Pathophysiology - increase sensitivity of tissues to insulin by activation of ppar-gamma receptor Benefit - longer duration of monotherapy - Mild blood pressure lowering - A1c lowering 0.8% - low risk of hypoglycemia Risks - weight gain - increased peripheral edema and heart failure - increased risk of fractures
Discuss the pathophysiology of insulin therapy
- bind to tyrosine kinase receptor on myocytes, hepatocytes, adipocytes to activate P13K -> PIP3 -> PDK/Akt signalling to ellicit
- increased glycogenesis, lipogenesis and triglyceride synthesis
- decreased lipolysis, glycogenolysis, and ketogenesis
- increase glucose uptake from blood
- liver and muscle increase glycogenesis and protein synthesis
- adipocytes inhibit lipolysis
Discuss the correction scale for insulin
- bolus prescribed by correction scale
- # units of insulin per # increase in pre-prandial blood sugar over # of calculated insulin for meal
Discuss the general principles of managing diabetes in hospital
- Type require insulin even if NPO
- diabetic diet
- BG monitoring at before meals, at night and prn
- Continue with pre-admission treatment and change if
- NPO or decreased PO intake
- HbAIc >8%
- measured BG >10
- frequent episodes of hypoglycemia
Discuss management of type 2 diabetic patients in hospital
Patients newly diagnosed (add in order below)
- Max dose oral agent
- add new oral agent from another class
- Start basal insulin
- 0.2-0.3 units/kg long acting (Glaring, Determir) at night or NPH before breakfast and at night
- Add meal time insulin
- discontinue all oral agents except metformin
- 0.1-0.2 units/kg of fast acting at breakfast, lunch supper if long acting or before breakfast and supper if on NPH
- Use corrective insulin sliding scale
- Adjust insulin based on glucose pattenr
- hypoglycemia: decrease at time before noticed
- adjust insulin to get pre-prandial breakfast into range
- correct insulin to correct for high insulin during the day
Patients on Insulin (add in order)
- start basal insulin (same as above)
- add meal time insulin (same as above)
- use corrective insulin sliding scale
- adjust as needed
Discuss the management of diabetic patients that are NPO or cannot take oral agents due to renal failure
Discontinue all oral agents
NPO/Clear Fluids
- CBG Q6H
- IV D5W 100cc/hr
- discontinue meal time insulin
- NPO >2days or peri-operative then IV protocol
- previously on oral agents/diet and not on insulin
- use corrective scale
- if >8 units after 2 days then start basal
- previously on insulin
- switch basal to 1/2 to 2/3 basal insulin dose
- use corrective
Discuss insulin use for patients on steroids
- cause hyperglycemia 5-12 hrs after steroid intake
Morning Steroid Only - NPH 0.2-0.4units/kg before breakfast
Steroid BID-QID - NPH 0.2-0.4 units/kg before breakfast and dinner
Discuss the presentation and management of hypoglycemia
Presentation
- autonomic/adrenergic symptoms
- hunger
- diaphoresis
- tremulousness, tingling
- palpitation
- anxiety
- Neuroglycopenic symptoms
- dizziness
- unusual behaviour
- seizure
- visual changes
- late type 1 and type 2 there is hypoglcyemia unawareness so less symptoms
Diagnosis
- Whipple's triad: blood glucose <2.8 with symptoms that is corrected with food or glucose
Management
- conscious eat food or drink with carbohydrate or 15-20g glucose tablet
- should improve in 5-10 and complete in <20
- Unconscious glucagon 1mg SC/IM or 50mL D50W
- thiamine 100mg IMList the 5 I’s of diabetic ketoacidosis
Insulin Deficiency - inadequate dose - omission of insulin - new diagnosis Infection - most common Ischemia - MI - stroke Intra-abdominal process - pregnancy - pancreatitis Intoxication - drugs or alcohol
Discuss the pathophysiology of diabetic ketoacidosis
Severe Insulin Deficiency
- stress increase insulin demand that is not matched by pancreas
- decrease peripheral glucose utilization and uptake, leading to hyperglycemia
- K shift out of cell leading to hyperkalemia with low body store of K
Severe Cell Starvation
- liver produce and release glucose -> hyperglycemia
- adipose tissue release free fatty acids which are converted to ketones by liver
- peripheral muscle decrease glucose utilization leading to weakness
Ketone Bodies
- cause metabolic acidosis, which can be compensated by breathing
Hyperglycemia and Ketone Bodies
- cause osmotic diuresis
- dehydration
- electrolyte depletion
- hyperosmolality (hyponatremia and cerebral dehydration)
Discuss the presentation, investigation and diagnosis of DKA
Presentation - sleepiness, LOC - blurry vision - N/V - polyuria, polydipsia - Kaussmaul breathing - hypovolemic - fruity ketone breath Investigation - CBC, electrolytes, creatinine BUN - blood glucose - serum osmolality - serum ketone - VBG - urine analysis - ECG Diagnosis (all of the following) - metabolic acidosis with increased anion gap - serum and urine ketone bodies - hyperglycemia
Discuss the management of DKA
- Q2-4H electrolytes, anion gap, glucose, creatinine, plasma osmolality, LOC
IV Fluids for decreased Effective Circulating Volume - Severe shock give NS 1-2L/h until hypotension correction and then switch to NS 500mL/hr for 4hr then 250mL/hr for 4 hr
- mild to moderate start at 500mL - Once euvolemic
- Na is normal/high or rate of plasma osmolality fall is <3 switch to 0.45NS
- Na is low or rate of plasma osmolality fall >=3 then continue with 0.9%NS - Once plasma glucose reaches 14 add D5W to IV fluids to maintain glucose 12-14
Serum K - <3.3 then give 40mmol/L KCl and no insulin until K >=3.3
- > =3.3 and less 5-5.5 then 10-40KCl
Acisosi - if K <3.3 correct hypokalemia before insulin
- if K >=3.3 administer IV short acting insulin 0.1unit/kg/h
- adjust rate of insulin based on anion gap resolution - if pH <7.0 then NaHCO3 1 amp/h until pH >=7
Differentiate between primary and secondary hypothyroidism
Primary
- thyroid gland not making enough thyroid hormone
- high TSH low T3/T4
- autoimmune hypothyroidism from Hashimoto’s
- iodine induced
- drug induced (amiodarone)
Secondary
- central where failure of pituitary stimulation of thyroid hormone
- low TSH and T3/T4
- pituitary disease (tumour)
Discuss the presentation, investigations to hypothyroidism
Presentation
- weight gain
- dry/itchy/cold/coarse skin
- hair loss
- fatigue
- cold intolerance
- depression, psychosis
- joint pain and muscle cramps
- muscle weakness
- constiptation
- menstrual irregularities and menorrhagia
- myxedema (non pitting edema)
- puffiness with coarse brittle hair (eyebrow)
- peri-orbucular swelling
- enlarged tongue
- goitre
- delayed deep tendon reflex
- carpal tunnel syndrome
- bradycardia and diastolic hypertension
Investigation
- TSH and Free T3/T4
- subclinical T4 may be normalDiscuss the management for hypothryoidism
Levothyroxine
- synthetic T4 (body can convert to T3)
- start at 1.7mcg/kg/d
- monitor response at 6 weeks
- primary target to TSH <5
- in pregnancy may require more and target is <2
Indications
- TSH >10
- Symptomatic
- Subclinical and pregnancy
- hypertension, hypercholesterolemiaDifferentiate between primary and secondary hyperthyroidism
Primary
- thyroid gland overproduce thyroid hormone despite good negative feedback loop
- TSH low and Free T3/T4 high
- autoimmune: Grave's
- toxic nodular goitre
- hyperthyroid phase of acute thyroidits
- excessive synthroid, amiodarone, iodine in diet
Secondary
- pituitary excrete excessive TSH
- high TSH and T3/T4
- pituitary adenomaDiscuss the presentation and investigations for hyperthyroidism
Presentation - heat intolerance, sweating, weight loss - anxiety, insomnia - palpitation - muscle aches, hyperactivity - frequent bowel movements - loss of libido - moist skin - tremor - diffuse goitre and bruit - tachycardia and systolic hypertension - palmar erythema, onycholysis - lid lag, proptosis - hyperreflexia - pretibial myxedema Investigation - TSH, T3/T4 - Radioactive Iodine Uptake
Discuss the findings of TSH, T3/T4, radioactive uptake and thyroglobulin for different causes of hyperthyroidism
Graves - low TSH - very High T3/T4 - very High Radioactive uptake Toxic Nodule - low TSH - high T3/T4 - high radioactive uptake Subacute thyroiditis - low TSH - high T3/T4 - low radioactive iodine uptake - high thyroglobulin Factitious Thyrotoxicosis - low TSH - high T3/T4 - low radioactive iodine uptake - low thyroglobulin TSH Secreting tumour - high TSH - high T3/T3 - high radioactive iodine uptake
Discuss the management of hyperthyroidism
Antithyroid Drugs
- Methimazole and Propylthiouracil
- inhibit thyroperoxidase
- PTU also inhibit deiodinase that convert T4 to T3
- PTU used in pregnancy
Radioactive Iodine
- cure Grave disease, multi nodular goitre or toxic nodule
- can not use in women if wanting to get pregnant in next 6 months
Subtotal surgical Thyroidectomy
- last line
Beta Blocker
- symptomatic
- propanololDifferentiate between different types of adrenal insufficiency
Primary
- decreased production of glucocorticoid from adrenal cortex
- Addison’
- TB, HIV
- congenital adrenal hypoplasia
Secondary
- Decreased ACTH from pituitary resulting in decreased glucocorticoid production from adrenal cortex
- hypopituitarism
- pituitary adenoma or stalk trauma
- suppression of ACTH from withdrawal of exogenous steroids
Tertiary
- decreased CRH from hypothalamus resulting in decreased ACTH
Discuss the presentation, diagnosis and treatment of chronic adrenal insufficiency
Presentation
- weakness, weight loss
- N/V
- hypotension and postural dizziness
- visual field defect if pituitary adenoma
- hyponatremia
- primary: dark skin and mucosa from ACTH, metabolic acidosis
- secondary: hypothyroidism and hypogonadism
Diagnosis
- low plasma cortisol at 8am or low plasma cortisol despite ACTH stimulation
- primary high ACTH and low cortisol and persistent low cortisol despite stimulation
- secondary/tertiary low ACTH and cortisol, increased cortisol in response to ACTH stimulation
Management
- hydrocortisone 15-20mg daily divided BID-TID
- increase 2-3x if mod-severe illness
- large dose 150-300mg IV daily divided TID for major stress (surgery, trauma)
- medical alert bracelet for IM hydrocortisone if suffer major stress
Discuss the presentation and management of adrenal crisis
- inappropriate cortisol production in response to stress
Presentation
- N/V
- confusion
- shock/hypotension
- hypoglycemia
Management
- obtain blood sample for ACTH, cortisol and electrolyte
- Immediate:
- IV NS 2-3L bolus
- D5W if hypoglycemic
- hydrocortisone 50-100mg IV Q6-8H for 24hr then taper
