Endocrinology Flashcards

(37 cards)

1
Q

Differentiate between macrovascular and microvascular complications with diabetes

A
Macrovascular
- medium and large size blood vessels involved
- CAD, MI, stroke, PAD
Microvascular
- involve small capillaries
- retinopathy, nephropathy, neuropathy
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2
Q

Discuss the stages of diabetic retinopathy

A

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

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3
Q

Discuss the presentation and management of diabetic retinopathy

A
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
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4
Q

Discuss the stages of diabetic nephropathy

A
- 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
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5
Q

Discuss the management of diabetic nephropathy

A
  • glycemic control
  • blood pressure control
  • ACEi or ARB to reduce albuminemia
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6
Q

Discuss the presentation of different types of diabetic neuropathy

A

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

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7
Q

Discuss the presentation, investigations and management for diabetic foot ulcer/cellulitis

A
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 + Ceftriaxone
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8
Q

Discuss classification of infection and risk for osteomyelitis for diabetic foot ulcer

A

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

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9
Q

Discuss the pathophysiology, benefits, risks and dosing of biguanides

A
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
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10
Q

Discuss the pathophysiology, benefits, risks and dosing of incretins

A
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
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11
Q

Discuss the pathophysiology, benefits, risks and dosing of DDP-IV inhibitors

A
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
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12
Q

Discuss the pathophysiology, benefits, risks and dosing of SGL2-inhibitors

A

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

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13
Q

Discuss the pathophysiology, benefits, risks and dosing of sulfonylurea

A
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
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14
Q

Discuss the pathophysiology, benefits, risks and dosing of meglitinide

A
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
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15
Q

Discuss the pathophysiology, benefits, risks and dosing of acarbose-glucosidase inhibitor

A
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
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16
Q

Discuss the pathophysiology, benefits, risks and dosing of thiazolidinediones

A
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
17
Q

Discuss the pathophysiology of insulin therapy

A
  • 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
18
Q

Discuss the correction scale for insulin

A
  • bolus prescribed by correction scale

- # units of insulin per # increase in pre-prandial blood sugar over # of calculated insulin for meal

19
Q

Discuss the general principles of managing diabetes in hospital

A
  • 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
20
Q

Discuss management of type 2 diabetic patients in hospital

A

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

21
Q

Discuss the management of diabetic patients that are NPO or cannot take oral agents due to renal failure

A

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

22
Q

Discuss insulin use for patients on steroids

A
  • 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
23
Q

Discuss the presentation and management of hypoglycemia

A
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 IM
24
Q

List the 5 I’s of diabetic ketoacidosis

A
Insulin Deficiency
- inadequate dose
- omission of insulin
- new diagnosis
Infection
- most common
Ischemia
- MI
- stroke
Intra-abdominal process
- pregnancy
- pancreatitis
Intoxication
- drugs or alcohol
25
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)
26
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 ```
27
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
28
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)
29
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 normal ```
30
Discuss 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, hypercholesterolemia ```
31
Differentiate 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 adenoma ```
32
Discuss 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 ```
33
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 ```
34
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 - propanolol ```
35
Differentiate 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
36
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
37
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 ```