Endocrine pharmacology Flashcards
1
Q
Diabetes mellitus diagnosis
A
- fast glucose >126
- 2 hr post prandial >200
- A1C >6.5
2
Q
Pre-diabetes levels for A1C and fasting glucose
A
- 5.7 - 6.5 A1C
- 100-120 fasting glucose
3
Q
Type 1 DM
A
- autoimmune destruction of beta-cells
- insulin deficient
- polyuria, polydipsia, DKA
- Hyperglycemia
4
Q
Type 2: DM
A
- majority of DM
- insulin resistant
- hyperglycemia
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
6
Q
DM Treatment
A
- education
- diet
- execise
- meds
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
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
9
Q
roll of the kidney in glucose homeostasis
A
- 90% of glucose reabsorption in kidney occurs by Na glucose Co-transporter in PCT
10
Q
non-insulin medication for diabetes: sulfonyurea; glipizide
A
- promotes insulin secretion
11
Q
non-insulin medication for diabetes: decrease hepatic gluconeogenesis
A
- metformin
- may need vitamin B12
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
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
14
Q
Hyperlipidemia
A
- association between atherosclerosis and lipids
- primary disturbances: genetics
- secondary disturbances: comes from diet
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
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
Therapeutic effects of glucocorticoid
- anti-allergic
- anti-inflammatory
- decrease pain
- decrease stiffness
- decrease disability
- decrease endothelial dysfunction and permeability
- decrease effect of RA on joint damage
26
adverse effects of glucocorticoid steroids
- 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
adverse effects of glucocorticoid steroids
- iatrogenic cushings
- adrenal suppression (avoid abrupt stop as it can cause Addisons)
- immunosuppressive effects
28
PT considerations for glucocorticoids (esp. injections)
- no forceful resistance 2 weeks after injection
- nothing can be directly put over area for 2 weeks such as a hot pack
29
indications for glucocorticoids
- Addisons disease (adrenal disorder)
- inflammatory conditions
- autoimmune disorders
- preventions and treatment of organ rejection
30
Describe bone mineral homeostasis
- 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
Endogenous regulators of Ca/bone mineral homeostasis
- Vitamin D
- PTH
- fibroblast growth factor 23
- calcitonin
- estrogens
- glucocorticoids
32
describe how vitamin D is involved in bone mineral homeostasis
- increase intestinal absorption and bone resorption of Ca and phosphate
- decrease renal excretion of Ca and phosphate
- serum Ca and phosphate increase
33
Describe how PTH is involved in bone mineral homeostasis
- 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
describe how Fibroblast Growth factor 23 is involved with bone mineral homeostasis s
- decrease intestinal Ca and phosphate absorption
- increase phosphate kidney excretion
- decrease serum phosphate
35
describe how Calcitonin is involved in bone mineral homeostasis
- secreted by thyroid
- inhibits bone mineral breakdown and renal reabsorption of Ca and phosphate
36
describe how Estrogen in involved in bone mineral homeostasis
- delay bone loss
- increase calcitriol in blood
37
describe how glucocorticoids are involved in bone mineral homeostasis
- block bone formation
38
Exogenous regulators of bone mineral density and how they are involved
- 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
PT considerations for exogenous regulators of bone mineral density
- benefit from resistance training
- pharmacology considerations: bisphosphonates can cause esophageal irritation so watch positioning if they have taken within 45 minutes
