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6-11 ENDOCRINE RENAL > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Action of ACTH

A
  1. act on adrenal glands to stimulate glucocorticoid release

2. also has a trophic effect on adrenal cortex

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2
Q

Effects of glucocorticoids

A

Metabolic: protein, CHO metabolism and adipose distribution
Anti-inflammatory
Resistance to stress

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3
Q

Effects of mineralocorticoids

A

Water and electrolyte homeostasis

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4
Q

Corticosteroid mechanism of action

A
  • Plasma cortisol - bound to CBG
  • Lipophilic molecule → crosses PM &
    binds cytoplasmic receptor (GR)
  • (Cortisol also binds MR)
  • GR dimerises & translocates to nucleus
  • Dimeric GR binds GREs to alter transcription of target genes
  • GR is a ligand-activated transcription factor
  • Transcriptional activation → most GC metabolic effects
  • Transcriptional repression → pro-inflammatory genes e.g. IL-2
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5
Q

Primary deficiency of corticosteroids

A

Addison’s disease

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6
Q

Secondary deficiency of corticosteroids

A
  • exogenous steroid use

leads to HPA axis suppression

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7
Q

Glucocorticoid XS

A

Cushing’s syndrome

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8
Q

Common signs of Cushing’s

A 
Catabolic:
-thin skin and striae
-bruising
-muscle wasting - thin arms & legs
Fat redistribution/deposition:
-moon facies 
-buffalo hump 
-abdominal
Cushingoid changes don’t only occur with systemic steroid administration → 2 years inhaled fluticasone
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9
Q

Clinical uses of GC’s

A
  1. replacement therapy

2. anti-inflammatory therapy (GC only)

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10
Q

Hyperthyroidism treatment strategies

A
  • remove gland and T4
  • inhibit thyroperoxidase
  • prevent peripheral deiodination of T4
  • interfere with sympathetic nervous system facilitating action of T3 and 4
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11
Q

Iodide as a treatment for hyperthyroidism

A
  • alpha and beta-emitter
  • Taken orally as an iodide salt
  • Actively incorporated by thyroid epithelium • -emission leads to death of thyroid tissue • t1⁄2~8days
  • Patient ultimately becomes hypothyroid
  • Then needs T4 replacement
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12
Q

What are some thiourylenes and how do they act?

A
  • carbimazole and methimazole
  • propylthiouracil
    They inhibit thyroperoxidase - prevents iodination of tyrosine residues and prevents conversion of T4 to T3
    They deplete the follicle contents over 3-4 weeks
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13
Q

Action of potassium iodide in hyperthyroidism

A

Suppresses release of stored thyroid hormone
Inhibits peripheral conversion of T3-T4

For fast and temporary suppression of hyperthyroidism

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14
Q

What is important in monitoring T4 replacement and anti-thyroid drugs?

A

TSH level most generally useful

High TSH = needs more T4 or less anti-thyroid

Low TSH = needs less T4 or more anti-thyroid

Free T4 measurement appropriate in some specific clinical situations

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15
Q

Action of beta adrenergic blockers in hyperthyroidism

A

Antagonises thyroid hormone facilitation of sympathetic activity.

Adjunct in managing hyperthyroid-related tachyarrhythmias

Suppresses sympathetic manifestations • Tachycardia
• Tremor
• Eyelid retraction

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16
Q

3 Zones of adrenal cortex and what they produce

A
  1. Zone glomerulosa = mineralocorticoids
  2. Zona fasciculate = glucocorticoids
  3. Zona reticularis = sex hormones
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17
Q

Rate limiting step in adrenal steroidogenesis

A

Side chain cleavage of cholesterol

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18
Q

How is insulin stored in the pancreas?

A

Stored as pro-insulin in beta cell granules and is then proteolytically cleaved into mature insulin + C-peptide

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19
Q

What stimulates insulin release?

A
  • glucose increase
  • amino acids and fatty acids
  • peptide gut hormones - incretins (GLP1, GIP, CCK)
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20
Q

What does insulin activate?

A
  1. GLUT4 transporter - glucose enters cells
  2. Glycogen synthase - converts glucose to glycogen
  3. cell growth and gene expression pathways
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21
Q

Presenting symptoms in diabetes

A 
o	Polyuria 
o	Polydipsia – thirst
o	Polyphagia – hunger 
o	Weight loss  catabolism
o	Tiredness, confusion, irritability
o	Poor healing and infections
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22
Q

Difference between type 1 and 2 diabetes

A

Type 1: absolute insulin deficiency / autoimmune destruction of B cells
Type 2: relative insulin deficiency / peripheral insulin resistance

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23
Q

Microvascular complications in the eyes and kidneys

A

Eyes
• Diabetic retinopathy

  • ↑ vascular permeability
  • haemorrhages
•	lipid exudates 
•	neovascularisation 
•	25x↑ in blindness 
•	cataracts, glaucoma 
Kidneys
•	Diabetic nephropathy 
•	Glomerular disease

• ↓ GFR & albuminuria

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24
Q

Treatment of diabetes type 1

A
  1. insulin
  2. diet, exercise and lifestyle
  3. regular monitoring
25
Q

Importance of HbAc1 in diabetes monitoring

A 
HbA1c: 
•	covalent modification of Hb - 
•	long term measurement of glucose levels 
•	4 - 6% - normal range 
•	<7% - good control 
•	>8% - poor control
26
Q

How is insulin administered normally and in emergency?

A

Normally S.C

Emergency I.V

27
Q

Side effects of insulin therapy

A

Hypoglycemia
Weight gain
Injection site - scarring, lipoatrophy/hypertrophy

28
Q

Treatment for type 2 diabetes

A

Aim: lower blood glucose levels to prevent microvascular complications

  1. Lifestyle measures
  2. oral hypoglycaemic agents
  3. insulin
  4. Treat associated conditions
29
Q

Hypoglycemic agents for T2DM

A
  1. Metformin
  2. Sulfonylureas

Also

  • Thiazolidinediones
  • α-Glucosidase Inhibitors
  • Incretin based therapies
  • SGLT2 inhibitors
30
Q

Mechanism of action of metformin

A
  • Mainly reduces hepatic gluconeogenesis
  • May also cause GLP1 release – incretin effect
  • Additional benefits – no hypoglycaemia, no increase in appetite, no weight gain, improved lipid profile, reduced CRC rates?
31
Q

Mechanism of action of slufonylureas

A

Mechanism of action: insulin secretagogues
• Bind SU receptor (SUR1) on beta cells to block K+ channel insulin release
• Need functional beta cells

32
Q

Side effects of metformin

A
  • GI 30% but transient – helps with weight control
  • Lactic acidosis – extremely rare
  • Vitamin B12 deficiency (reduced absorption?) – screen your patients!
  • C/I in severe renal, hepatic or cardiac failure
33
Q

Mechanism of action of Thiazolidinediones

A
  • PPARγ nuclear receptor expressed in many tissues
  • PPARγ agonists activate gene transcription
  • Increase in insulin sensitivity (30%) – effects take weeks to months to develop
  • Also improve lipid profiles
34
Q

What are incretins and how are they involved in diabetes and management?

A

Incretin: gut peptide that increases insulin release after food (oral glucose not IV)
Incretin response is decreased in T2D
Incretin based therapies: increase insulin release in a glucose dependent manner
- GLP1 receptor agonists
- DPP-4 inhibitors

35
Q

Which drugs are really eliminated and have a narrow therapeutic range?

A
  • Aminoglycoside antibiotics (eg gentamicin)
  • Factor Xa & Prothrombin Inhibitors (-gatran’s & -aban’s)
  • Digoxin, atenolol, some ACE-inhibitors, eg ramipril
  • Lithium
•	Hypoglycaemics: metformin, insulin -
some sulphonylureas (glibenclamide)
  • Methotrexate
  • Allopurinol (in people genetically predisposed to immune-mediated toxicity)
  • Nitrofurantoin (urinary antibacterial)

Antiviral“cyclovirs”(egaciclovir,ganciclovir)

36
Q

Why is it important to measure creatinine clearance?

A
  • get a good idea of renal function
  • track changes in renal function over time
  • roughly estimate renal clearance for common drugs
37
Q

Really eliminated toxic metabolites

A

¥ Morphine 6-glucuronide sedation

¥ Pethidine norpethidine seizures (part of the reason why pethidine is never a drug of choice)

38
Q

Drugs which have altered pharmacokinetics in renal disease

A

Reduced efficacy
- diuretics

Increased toxicity

  • K+ sparing diuretics
  • Anticoagulants
  • CNS depressants more sedating
  • Diuretics, NSAIDs and ACE inhibitors or Angiotensin receptor blockers more likely to affect GFR
39
Q

How do MR tissues respond to aldosterone not cortisol?

A

They express 11-beta-steroid hydrogenase which converts cortisol to cortisone (not active)

40
Q

What does GC and MC deficiency affect in Adison’s?

A

GC: CHO metabolism = reduced glucose and impaired stress tolerance = Adisonian crisis
MC: reduced BP, low sodium, high potassium

41
Q

What is preserved in secondary deficiency of corticosteroids?

A

MC secretion = normal RAAS / normal BP / normal NA+/K+ balance

42
Q

Differentiating between primary and secondary adrenal insufficiency

A

Secondary has normal K+/Na+, ACTH is low normal so no pigmentation change, rapid ACTH test will differentiate

43
Q

Causes of cushion’s syndrome

A
  1. Cushing’s disease = raised ACTH from ALP
  2. Raised ACTH from ectopic source
  3. Increased GC from adrenal carcinoma/adenoma
  4. Increased GC from prescribed GC = iatrogenic
44
Q

Treatment of adrenocortical insufficiency

A

MEDICAL EMERGENCY

  • IV hydrocortisone
  • then hydrocortisone to replace diurnal rhythm
  • during times of stress - double the dose of hydrocortisone
45
Q

Corticosteroid AEs

A
  1. Iatrogenic cushion’s syndrome
    - Very common with systemic GC use, patents look cushingoid and children have growth suppression
  2. Suppression of HPA axis
    - adrenal atrophy may occur and abrupt GC withdrawal may result in Adisonian crisis
46
Q

Action of TSH

A
  1. increase BF to thyroid
  2. Increase uptake of iodine into thyroid
  3. Increase iodination of tyrosine on thyroglobulin
  4. Increases formation of thyroglobulin-associated T3 + T4
  5. Increases release of stored T3 + T4
47
Q

Effects of thyroid hormones

A

Growth and maturation
Increased metabolic rate
Adrenergic facilitation

48
Q

Causes of hypothyroidism

A
  1. AI thyroid disease
  2. iodine deficiency
  3. surgical removal or radio-iodine treatment
  4. drug induced
49
Q

Causes of hyperthyroidism

A
  1. Grave’s disease
  2. Thyroid adenoma
  3. Thyroid hypertrophy
  4. Overproduction of TSH - rare
50
Q

Which hormones increase and decrease blood glucose levels?

A

Increase: glucagon, adrenaline, glucocorticoids, growth hormone
Decrease: insulin

51
Q

Action of insulin on carbohydrates in the liver, muscle and fat

A

Liver: increase glycolysis and glycogenesis. Decrease gluconeogenesis and glycogenolysis.

Muscle: increase glucose uptake and glycolysis

Fat: increase glucose uptake and glycerol synthesis

52
Q

Diagnosis of Diabetes

A

Fasting glucose >7mmol/L

2hr post prandial >11.1mmol/L

53
Q

What causes diabetic foot ulcers?

A

Neuropathy: sensory can’t feel pain OR motor - foot deformities
PVD - ischaemic ulcers
Immunosuppresion - infections

54
Q

Metformin mechanism of action

A

Hypoglycemic agent - Reduces hepatic gluconeogenesis

55
Q

Mechanism of action of sulfonylureas

A

Insulin secretagogues:
Binds SUR1 receptor on beta cells to block K+ channel which stimulates insulin secretion

–> Requires functional beta cells

56
Q

Action of thiazolidinediones

A

PPAR-gamma agonist - activates gene transcription

Results in increased insulin sensitivity and improves lipid profiles

57
Q

Mechanism of action of alpha-glucosidase inhibitors

A

Competitive inhibitor of intestinal alpha-glucosidase
Inhibits breakdown of maltose into glucose
Delay CHO absorption –> controls post prandial hyperglycaemia
Regularly prescribed with metformin and sulfonylureas

58
Q

Action of SGLT2 inhibitors: Dapagliflozin

A

> 90% of glucose is reabsorbed by SGLT2 in PCT
Inhibitor prevents glucose reabsorption/ and salt
Results in:
- glycosuria
- reduced BGL
- Reduced BP
- Reduced weight

6-11 ENDOCRINE RENAL (7 decks)

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