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Medical Conditions 2 > Endocrine pharmacology > Flashcards

Endocrine pharmacology Flashcards

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USMLE® Step 1 flashcards
1
Q

Diabetes mellitus diagnosis

A
  • fast glucose >126
  • 2 hr post prandial >200
  • A1C >6.5
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2
Q

Pre-diabetes levels for A1C and fasting glucose

A
  • 5.7 - 6.5 A1C
  • 100-120 fasting glucose
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3
Q

Type 1 DM

A
  • autoimmune destruction of beta-cells
  • insulin deficient
  • polyuria, polydipsia, DKA
  • Hyperglycemia
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4
Q

Type 2: DM

A
  • majority of DM
  • insulin resistant
  • hyperglycemia
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5
Q

Goals: for DM

A
  • A1C < 7%
  • premeal glucose 90-130 mg/dL
  • post meal (prandial): 1 hr <180; 2 hr <150 mg/dL
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6
Q

DM Treatment

A
  • education
  • diet
  • execise
  • meds
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7
Q

describe glucose homeostasis in response to increase in blood glucose levels

A
  • pancreas Beta cells release insulin into the blood
  • insulin causes body cells and liver to take up glucose
  • gut hormones (incretins GLP-1 and GIP) stimulate endogenous insulin
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8
Q

describe glucose homeostasis in response to blood glucose falling

A
  • alpha cells of the pancreas release glucagon
  • glucagon stimulates the liver to break down glycogen to release glucose
  • blood glucose rises
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9
Q

roll of the kidney in glucose homeostasis

A
  • 90% of glucose reabsorption in kidney occurs by Na glucose Co-transporter in PCT
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10
Q

non-insulin medication for diabetes: sulfonyurea; glipizide

A
  • promotes insulin secretion
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11
Q

non-insulin medication for diabetes: decrease hepatic gluconeogenesis

A
  • metformin
  • may need vitamin B12
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12
Q

non-insulin medication for diabetes: modulate incretins

A
  • GLP-1 receptor agonist/DPP4 inhibitors
  • feel fuller longer
  • ozempic, wagvy
  • works on GLP and slows down emptying of the GI system
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13
Q

non-insulin medication for diabetes: Inhibit glucose reabsorption in kidney

A
  • jardiance
  • works on kidney to increase glucose in the bladder
  • having glucose in the bladder increases risk of UTI
  • educate to drink more water
  • reduces risk of heart and kidney disease
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14
Q

Hyperlipidemia

A
  • association between atherosclerosis and lipids
  • primary disturbances: genetics
  • secondary disturbances: comes from diet
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15
Q

optimal levels of cholesterol and triglycerides

A
  • total cholesterol: <160 (200)
  • LDL <100 (140)
  • triglycerides: <150
  • HDLs <40 increases risk
  • HDLs >60 mitigates CV risk
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16
Q

Medications for hyperlipidemia

A
  • statins
  • resins
  • ezetimibe
  • niacin
  • fibrates
  • PCSK 9 inhibitors
17
Q

Statins

A
  • HMG-CoA reductase inhibitors in liver
  • decreases cholesterol synthesis in the liver
  • 1st line of therapy
  • watch for myoapathies/rhabdomylsis
18
Q

resins

A
  • bind the bile acids
  • constipation common side effect
  • not used as much
19
Q

Ezetimibe

A
  • hyperlipidemia med
  • block the absorption of cholesterol from the food you eat
  • used as add on with statins
  • causes soreness but not as likely as statins
20
Q

Niacin

A
  • hyperlipidemia med
  • need high does for small reduction
  • ADR - flushing
  • both cholesterol and triglyceride lowering
21
Q

Fibrates

A
  • hyperlipidemia med
  • triglyceride lowering
  • when combined with statins increase risk of soreness
  • reserved for triglycerides >1000
22
Q

PCSK9 inhibitors

A
  • monoclonal antibodies
  • new added to statins
  • lower LDL
  • injection
  • often reserved if not reaching goal or soreness with others-
23
Q

What is the rule with how often steroids can be given

A
  • should not be given more than once every 4-6 weeks
  • no more than 4/ year
24
Q

examples of corticosteroid medications

A
  • hydrocortisone
  • prednisone
  • dexamethasone
  • beclomethasone/budesonide
  • triamcinolone and methylprednisdone
  • fludrocortisone
25
Q

Therapeutic effects of glucocorticoid

A
  • anti-allergic
  • anti-inflammatory
  • decrease pain
  • decrease stiffness
  • decrease disability
  • decrease endothelial dysfunction and permeability
  • decrease effect of RA on joint damage
26
Q

adverse effects of glucocorticoid steroids

A
  • increase risk of infections
  • myopathy
  • risk of osteonecrosis/osteoporosis
  • neuropsychiatric symptoms
  • weight gain
  • impaired glucose metabolism
  • insulin resistance
  • b-cell dysfunction
  • gastric ulcers if used with NSAIDs
  • hirsutism/skin thinning
  • cataract glaucoma
  • increase CVD risk
27
Q

adverse effects of glucocorticoid steroids

A
  • iatrogenic cushings
  • adrenal suppression (avoid abrupt stop as it can cause Addisons)
  • immunosuppressive effects
28
Q

PT considerations for glucocorticoids (esp. injections)

A
  • no forceful resistance 2 weeks after injection
  • nothing can be directly put over area for 2 weeks such as a hot pack
29
Q

indications for glucocorticoids

A
  • Addisons disease (adrenal disorder)
  • inflammatory conditions
  • autoimmune disorders
  • preventions and treatment of organ rejection
30
Q

Describe bone mineral homeostasis

A
  • decrease Ca in blood
  • increase in PTH
  • PTH increases calcitriol which increase Ca reabsorption
  • Calcitriol also increases mobilization of Ca from bone and increased absorption from the GI
31
Q

Endogenous regulators of Ca/bone mineral homeostasis

A
  • Vitamin D
  • PTH
  • fibroblast growth factor 23
  • calcitonin
  • estrogens
  • glucocorticoids
32
Q

describe how vitamin D is involved in bone mineral homeostasis

A
  • increase intestinal absorption and bone resorption of Ca and phosphate
  • decrease renal excretion of Ca and phosphate
  • serum Ca and phosphate increase
33
Q

Describe how PTH is involved in bone mineral homeostasis

A
  • increases intentional absorption and bone resorption of Ca and phosphates
  • decrease renal excretion of CA and increase renal excretion of phosphate
  • serum CA increases and phosphate decreases
34
Q

describe how Fibroblast Growth factor 23 is involved with bone mineral homeostasis s

A
  • decrease intestinal Ca and phosphate absorption
  • increase phosphate kidney excretion
  • decrease serum phosphate
35
Q

describe how Calcitonin is involved in bone mineral homeostasis

A
  • secreted by thyroid
  • inhibits bone mineral breakdown and renal reabsorption of Ca and phosphate
36
Q

describe how Estrogen in involved in bone mineral homeostasis

A
  • delay bone loss
  • increase calcitriol in blood
37
Q

describe how glucocorticoids are involved in bone mineral homeostasis

A
  • block bone formation
38
Q

Exogenous regulators of bone mineral density and how they are involved

A
  • biphosphonates: prevent osteoclasts and prevent osteoporosis, pagets disease, hypercalcemia
  • denosumab: monoclonal antibody, inhibits osteoclast formation, osteoporosis, limit bone metastases growth or bone loss
  • fluoride
  • calcimimetics: mimic Ca (lowering PTH)
  • thiazide diuretics: increase Ca excretion
39
Q

PT considerations for exogenous regulators of bone mineral density

A
  • benefit from resistance training
  • pharmacology considerations: bisphosphonates can cause esophageal irritation so watch positioning if they have taken within 45 minutes

Medical Conditions 2 (22 decks)

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