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Internal Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

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
Q

Discuss the pathophysiology of diabetic ketoacidosis

A

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
Q

Discuss the presentation, investigation and diagnosis of DKA

A 
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
Q

Discuss the management of DKA

A
  • 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
Q

Differentiate between primary and secondary hypothyroidism

A

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
Q

Discuss the presentation, investigations to hypothyroidism

A 
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
Q

Discuss the management for hypothryoidism

A 
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
Q

Differentiate between primary and secondary hyperthyroidism

A 
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
Q

Discuss the presentation and investigations for hyperthyroidism

A 
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
Q

Discuss the findings of TSH, T3/T4, radioactive uptake and thyroglobulin for different causes of hyperthyroidism

A 
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
Q

Discuss the management of hyperthyroidism

A 
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
Q

Differentiate between different types of adrenal insufficiency

A

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
Q

Discuss the presentation, diagnosis and treatment of chronic adrenal insufficiency

A

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
Q

Discuss the presentation and management of adrenal crisis

A 
- 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

Internal Medicine (12 decks)

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