Endocrine Flashcards

1
Q

Name 3 examples of systemic cortiosteroids and 3 indications for their use:

A
  • prednisolone, hydrocortisone, dexamethasone
  • to treat allergic or inflamm disorders (anaphylaxis, asthma)
  • supress autoimmune disease e.g. IBD, arthritis
  • to treat some cancers (as part of chemo/to reduces tumour swelling)
  • hormone replacement in Adrenal insufficiency or hypopituitarism
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2
Q

Corticosteroids MOA..bind to ____ receptors which ___ to the ___ and bind to _____-response elements that regulate ____ expression. They upregulate ___-_____ ___ and down-regulate ___-_____ ___.
They also suppress circulating ___ and __.
Metabolic effects include increased ____ from increased circulating amino and fatty acids released by catabolism of __ and fat.
Also have ______ effects, stimulating Na+ and water ___ and K+ ___ in the renal tubule

A
  • glucocorticoid receptors –> translocate to nucleus, bind to glucocorticoid-REs
  • regulate gene expression, upreg anti-inflamm genes, downreg. pro-inflamm genes
  • supress circulating monocytes and eosinophils
  • increased gluconeogenesis (from catabolism of muscle and fat)
  • mineralocorticoid effect, Na+/water retention and K+ excretion
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3
Q

Name 8 important adverse effects that may arise from systemic corticosteroid therapy
(think about MOA to remember these)

A
  • immunosuppression
  • metabolic effects: DM, osteoporosis
  • increased catabolism: proximal muscle weakness, skin thinning, easy bruising, gastritis
  • mood/behaviour: insomnia, confusion, psychosis, suicidal ideation
  • mineralocorticoid effects: HT, hypokalaemia, oedema
  • adrenal atrophy in prolonged rx (–> addisonian crisis on sudden withdrawal..fatigue, weight loss, arthralgia)
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4
Q

What 2 medication classes should be considered alongside long-term systemic corticosteroid therapy to reduce adverse effects?

A
  • bisphosphonates

- PPIs

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5
Q

When should you exercise caution in prescribing systemic corticosteroids?

A
  • people with an infection

- children (can supress growth)

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6
Q

corticosteroids increase the risk of peptic ulcers/GI bleeding when used with ____
and enhance hypokalaemia when used in pts also taking __-agonists, th____, ___ or ___ diuretics.
Efficacy can be reduced by cytochrome P450 inducers such as….

A
  • NSAIDS
  • B2 agonists, theophylline, loop or thiazide
  • rifampicin, phenytoin, carbamazepine
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7
Q

In a pt undergoing long-term systemic corticosteroid therapy who becomes acutely ill, what should you do with their dose while unwell and then once recovered?

A

(atrophic adrenal glands won’t be able to increase cortisol in response to stress - do this artificially)

  • double the dose during acute illness
  • reduce back to maintenance dose on recovery
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8
Q

Dipeptidyl peptidase 4 inhibitors are used in combo w Metformin for T2DM. What is the suffix for this class and by what mechanism to they exert their effects?

A

__gliptin e.g. sitagliptin, linagliptin

  • incretins (GLP1 and GIP) are rapidly inactivated/hydrolysed by DDP-4
  • inhibitors of this enzyme increase plasma conc of active incretins
  • incretins promote insulin secretion and suppress glucagon release so lower BM
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9
Q

DPP-4 inhibitors e.g. sitagliptin, main SEs include:

-and <1 % develop acute _____ (suspect if persistent ___ pain)

A

SEs: GI upset, headache, nasopharyngitis, peripheral oedema

-<1%: acute pancreatitis, persistent abdo pain

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10
Q

Give 3 CIs for the use of DPP-4 inhibitors e.g. sitagliptin

NB: caution in elderly, those w pancreatitis hx or renal impairment

A
  • CI: HISTORY OF HYPERSENSITIVITY TO CLASS
  • CI: TYPE 1 DIABETES TREATMENT
  • CI: KETOACIDOSIS
  • CI: PREGNANCY
  • CI: BREAST FEEDING
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11
Q

DPP-4 inhibitors e.g. sitagliptin efficacy and use is done via HbA1 results:
-if used as monotherapy target HbA1c is

A
  • aim <48 mmol if monotherapy
  • <53 mmol if with metformin
  • if remains >58 mmol add on
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12
Q

Name 3 effects insulin has on processes:

A
  • stimulates glucose uptake
  • stimulates glycogen, lipid and protein synthesis
  • inhibits gluconeogenesis and ketogenesis
  • drives K+ into cells
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13
Q

Suggest one serious SE of insulin rx and one more cosmetic SE

A
  • HYPOGLYCAEMIA (can -> coma/death), higher risk in renal impairment (less clearance)
  • lipohypertrophy at site of repeated injection
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14
Q

Concurrent insulin use with other hypoglycaemic agents increases risk of hypoglycaemia. Concurrent use with what common drug class requires insulin doses to be increased?

A

-concurrent corticosteroid use

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15
Q

Metformin is a biguanide that lowers blood glucose mainly by reducing what? as well as what effect on muscle?

A
  • reduces hepatic glucose output (glycogenolysis and gluconeogenesis)
  • increased glucose uptake and use by skeletal muscle
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16
Q

Can monotherapy with metformin cause hypoglycaemia ?

NB: metformin can cause weight loss

A

-Nope

17
Q

Suggest a common SEs of metformin use?

A
  • GI upset: nausea, vomiting, taste disturbance, anorexia, diarrhoea
  • rarely lactic acidosis
18
Q

What organ excretes metformin

A

-kidney

19
Q

if eGFR is

A
  • <30mL/min
  • stop in AKI
  • stop if severe tissue hypoxia (e.g. sepsis, cardio/resp failure, MI)
20
Q

Due to risk of hypoglycaemia, metformin should be withheld in acute ____ _____ and used caution in patients with chronic ____ ____

A
  • acute alcohol intoxication

- chronic alcohol abuse

21
Q

Metformin must be withheld before and for 48hrs after injection of what and why?

A
  • IV contrast media

- as increased risk of renal impairment, metformin accumulation and lactic acidosis

22
Q

Metformin and GI SEs when starting, how is best to manage?

A
  • start on a low dose, increase gradually e.g. 500mg once daily
  • swallow tablets whole with a glass of water, with or after food to minimise SEs
23
Q

Metformin efficacy is assessed via HbA1 results:

  • if used as monotherapy target HbA1c is < ____
  • if used in combo with other drugs, target is ____ triggers an add on therapy
A
  • aim <48 mmol if monotherapy
  • <53 mmol if used in combo
  • if remains >58 mmol add on
24
Q

What blood test should be measured before starting Metformin? And repeated at least annuallly?

A

-U&Es to check renal function

if RF or deteriorating kidney function, repeat more regularly

25
Q

Gliclazide is an example of what type of drug used to treat T2DM either with Metformin, or alone (if CI to metformin)

A

-Sulphonylurea

26
Q

Sulphonylureas e.g. g_____ lower blood glucose by stimulating what?
They block which channels where leading to cell membrane depolarisation and opening of which channels, leading to increased intracellular ___ conc, so stimulates _____ _____

A
  • gliclazide
  • stimulates pancreatic insulin release
  • block ATP-dependent K+ channels in beta-islet cell membranes
  • so voltage gated Ca2+ channels open, increased Ca2+ conc
  • stimulates insulin secretion
27
Q

Sulphonylureas are only effective in pts with _____ ____ function. And as insulin is an anabolic hormone and this drug class stimulates it’s secretion what is an adverse effect of this drug class use?

A
  • residual pancreatic function

- weight gain

28
Q

Give 2 SEs of Sulphonylureas (gliclazide)

A
  • GI upset: N&V, diarrhoea, constipation
  • Hypoglycaemia
  • Rare hypersensitivity reactions: hepatic toxicity, agranulocytosis
29
Q

Sulphonylureas (gliclazide) cautions: suggest 1

A
  • hepatic impairment
  • renal impairment
  • those at increased risk of hypoglycaemia
30
Q

What medication class can mask symptoms of hypoglycaemia in patients on Sulphonylureas (gliclazide):

A

-Beta-blockers

31
Q

What communication points are important to get across when commencing a pt on any anti-diabetic drug?

A
  • x has been prescribed as a long-term therapy to control BM and reduce the risk of diabetic complications e.g. micro/macro eye, kidney, heart
  • tablets aren’t replacement for lifestyle, keep exercise and good diet
  • warn of hypo sx (dizzy, nausea, sweating, confusion), take sugar then starchy snack if happens and seek medical advice if recurs
32
Q

Give 4 actions of insulin

A
  • stimulates glucose uptake from circulation-> tissues
  • increases use of glucose for energy
  • stimulates glycogen, lipid and protein synthesis
  • inhibits gluconeogenesis
  • inhibits ketogenesis
  • drives K+ into cells
33
Q

Where IV insulin is required what type is chosen
(e.g. rapid acting=immediate action, short duration, short acting = early onset, short duration, intermediate acting = intermediate action and duration or long acting - flat profile w regular administration)

A

-short acting e.g. Actrapid, it is a soluble insulin

34
Q

Typical daily insulin requirements are roughly how many units? (varies on weight, diet, activity and insulin resistance)

A

-30 to 50 units

35
Q

In diabetic emergencies/peri-op glycaemic control, a 1 unit/m: IV solution is made by diluting Actrapid __ units in __% ____ ____ __mL
(vs. in hyperkalaemia rx is roughly Actrapid 10units is given in 20% dextrose 100mL over 15mins)

A

-50 units in 0.9% sodium chloride 50 mL

36
Q

If insulin is given as a continuous IV infusion, what should be measured every 4hrs to guide need for replacement?

A

measure serum K+