Metabolic Flashcards

(85 cards)

1
Q

Examples of human insulins that are short acting

A
  • actrapid
  • humulin S
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2
Q

Short acting insulin analogues

A
  • humalog
  • novorapid
  • apidra
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3
Q

Short acting insulin normally used at mealtimes in conjunction with carb monitoring as 1 unit per 10g of carbohydrate

A
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4
Q

Example of long acting insulin

A

Levemir
Lantus
Adding other constituents to thee basic structure of insulin to slow down its breakdown at injection site

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5
Q

What is DAFNE

A

Dose adjustment for normal eating

Carb counting to adjust dose of units of insulin

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6
Q

What consideration before prescribing metformin

A
  • if eGRF less than 45ml/min then adjust dose and if less than 30 stop
  • stop in AKI as accumulates
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7
Q

What is the small risk of using metformin

A
  • lactic acidosis in patients with acute illness or aki as build of lactate occurs
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8
Q

For patients with high CVD risk T2 DM or chronic heart failure what needs to be given other than metformin

A
  • SGLT2 - inhibitors like dapaglifozins

If with duo therapy it doesn’t work - try other class of drugs

-l last resort is insulin but since is anabolic causes weight gain thus increasing CVD risk

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9
Q

Side effects of pioglitazones

A
  • weight gain
  • hypoglycaemia
  • oedema
  • heart failure
  • increased risk of bladder cancer
  • increase risk of small Bone fractures in women
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10
Q

Downside to DPP4 inhibitors

A

Low potency

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11
Q

Risks associated GLP-1 analogues

A
  • increased risk of pancreatitis

GI SE = N+V

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12
Q

Which anti-diabetic drug class is cardioprotective and renoprotective

A
  • sglt2- inhibitors
    ( but shouldn’t be used in DKA patients as increases euglycaemic DKA
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13
Q

What is needed for diagnosis of DKA

A
  • hyperglycaemia - >11

Ketones higher than 3

Acidameia - pH less than 7.3 or bicarbonate less than 15

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14
Q

In DKA what kind of insulin is given

A
  • fixed rate insulin infusion

But fluid resus should occur first as 1) would be perfusing kidney and also helps to dilute blood sugar) 2) if give insulin first it will move glucose form blood to cells and water will follow and lead to further dehydration and hypotension

Also need to give potassium at some point as action of above two will lead to plasma hypokalemia (arrhythmias…)

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15
Q

How is HHS different to DKA

A
  • IV fluids major key here as they already have endogenous insulin. Main problem here is that blood is too hyperglycaemic and hypovolemic
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16
Q

What is the range for hypoglycaemia

A
  • blood capillary less than 4
  • if patient not able to swallow use glucogel at buccal mucosa

If aggressive and too confused and you have IV access do that or not glucagon IM

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17
Q

what is the primary drug to alleviate symptoms of hyperthyroid

A
  • beta blockers non selective such as propranolol
    (also act to decrease peripheral conversion of T4 to T3)
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18
Q

carbimazole MOA

A
  • decreases production of thyroid hormone through affecting iodide conversion to iodine in follicular cells which is then stored in colloid. hormones are bound to thyroglobulin
    (T4 is major hormone produced in thyroid)

inhibits enzyme such as thyroid peroxidase

+ but takes long to work as pre-existing store of T4 has long life of 4-6 weeks

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19
Q

iodides can also be used

A
  • blocks the production and release of hormones from thyroid
  • cannot be used long term though 2-3 weeks
  • used in surgery
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20
Q

what is the alternative to carbimazole for pregnant women

A
  • propylthiouracil PTU
  • PTU inhibits peripheral conversion of T4 to T3
  • half life of PTU is shorter so more times needed in day (3)

however PTU can cause severe hepatic failure

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21
Q

other cautions associated with anti - thyrotoxicosis drugs

A
  • agranulocytosis
  • rashes and anaemia
  • hepatic failure with PTU
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22
Q

treatment of thyrotoxicosis regimens

A

1) Block and replace (shorter duration of treatment)

2) titration ( low dose to begin with?)

cant use block and replace in pregnancy

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23
Q

other anti-thyroid treatment alternatives

A

1) radioactive iodine
2) thyroidectomy

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24
Q

before radioiodine is given why is carbimazole given

A

-

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25
deficiency in ACTH: drug
- hydrocortisone
26
deficiency in GH
not required in adults
27
deficiency in TSH: drug
- levothyroxine
28
deficiency in LH and FSH: drug
testosterone - men HRT for women
29
sick day rules for steroids
- up the dose
30
management of addisonian crisis
- IV fluids - hydrocortisone ( at high concs also has mineralocorticoid actuvity) - prevent hypoglycaemia
31
treatment for high prolactin
cabergoline - dopamine agonist (dopamine is a tonic inhibitor of prolactin) or bromocriptine but more N+V side effects
32
treatment of severe hypocalcemia
calcium gluconate * Mg is needed for production and release of PTH
33
treamtnet for hypercalcemia
- lots of IV fluids as dehydrated - IV zolendronic acid (bisphosphonate) - steroids
34
MOA of bisphosphonates
- inhibit attachment of osteoclasts to bone thus inhibting bone resoprtion
35
moa of cinacalcet
- mimics calcium on PTH receptors so gland thinks too much calcium so reduces secretion of PTH
36
treatment for severe hyponatremia
- hypertonic saline
37
tolvaptan
V2 receptor antagonist - blocks action of ADH
38
use of tolvaptan
- PKD - SIAD
39
sick day rules for T1 DM
- never stop basal insulin - try and drink sugar free liquids at rate of 100ml/hr - if BG between 10-13 = increase insulin by 10% + check every 4hrs. if not improved by 24hrs increase again by 10% - If BG >13 increase usual inuslin by 10% and give extra dose of quick acting insulin - repeat every 2-4hrs
40
What non-pharmacological approaches might be considered in managing acute kidney injury?
hydration management, dietary modifications, monitoring of renal function, and avoiding nephrotoxic agents.
41
AKI actions
initial assessment: 1) ABCDE 2) Obs 3) signs of sepsis 4) abdo palpation for full bladder initial treatment: 1) sepsis 6 2) fluid regime if hypotensive 3) med review (stop drugs or lower dose) 4) relieve obstruction
42
in AKI why is serum K raised
Decreased Renal Potassium Excretion (Primary Mechanism) The kidneys normally excrete 90% of daily potassium intake. In AKI, there is a reduced glomerular filtration rate (GFR) → decreased K⁺ filtration and secretion.
43
which classes of drugs interfere with renal perfusion
1) ACEis 2) ARBS 3) NSAIDs
44
in AKI which drugs require dose reduction or cessation
- required as these are metabolised or excreted by the kidneys and may build up in AKI 1)LMWH 2) opiates 3) penicillin based antibiotics 4) sulfonylurea eg gliclazide 5) aciclovir (antivirals) 6) metformin
45
which drugs require close monitoring in AKI
1) WARFARIN 2) AMINOGLYCOSIDES 3) LITHIUM
46
which drugs aggravate hyperkalemia by blocking renal excretion
1) trimethoprim 2) spironolactone 3 ) amiloride
47
What non-pharmacological approaches can be used in managing chronic kidney disease?
Non-pharmacological approaches for managing CKD include dietary modifications, fluid management, and lifestyle changes such as smoking cessation and exercise.
48
how might you alter a prescription of a drug that is mostly excreted through kidneys in a patient with significant renal impairment
1) Loading dose (first dose): Usually remains unchanged because distribution is not affected by renal function. Maintenance dose (subsequent doses): Often reduced, since clearance is impaired. 2) extend dosing interval if drug has longer half life 3) monitor drug levels 4) use alternative options
49
management of uncomplicated lower UTI
Non-Pharmacological Approaches Hydration: Encourage increased fluid intake to help flush out bacteria. Voiding Habits: Advise frequent urination and post-coital urination. Cranberry Products: May reduce recurrence in some patients. Avoid Bladder Irritants: Reduce caffeine, alcohol, and spicy foods. B. Pharmacological Treatment First-line Antibiotics (Empirical Treatment, Duration: 3 Days in Women, 7 Days in Men) Antibiotic Dose & Duration Comments Nitrofurantoin 100 mg PO BD for 5 days Trimethoprim 200 mg PO BD for 3 days Fosfomycin 3 g PO 🔹 Alternative (if resistance/allergy): Pivmecillinam 400 mg PO TDS for 3–5 days. 🔹 Avoid ciprofloxacin or levofloxacin due to resistance concerns.
50
management of pyelonephritis
Non-Pharmacological Approaches Adequate Hydration: IV fluids may be needed if vomiting or hypotensive. Pain Management: Paracetamol; avoid NSAIDs (can worsen renal function). oral: 1) cipro 2) co amoxiclav 3) co-trim IV: - ceftriaxone - pip-taz - gentamicin
51
facts about gentamicin
- nephrotoxic - ototoxic - 30s inhibitor - is hydrophilic - given IV or IM (not readily absorbed by GI tract)
52
Define the pharmacokinetics of gentamicin regarding its distribution in the body.
Gentamicin is highly hydrophilic, meaning it is not distributed into body fat and is minimally distributed into tissue fluids. Dosing calculations typically use the lower of actual or ideal body weight.
53
Explain the elimination process of gentamicin from the body.
Gentamicin is excreted unmodified by the kidneys and follows first-order elimination kinetics, conforming to a single compartment model with a single exponential curve of concentration over time.
54
Explain the purpose of the Hartford nomogram in gentamicin dosing.
The Hartford nomogram is used to determine the dosing interval for gentamicin based on the patient's serum concentration of the drug. It helps in adjusting the dose frequency according to the measured levels.
55
Define the types of urinary incontinence.
1. Urgency urinary incontinence - associated with overactive bladder syndrome. 2. Stress urinary incontinence - due to urethral sphincter incompetence. 3. Mixed urinary incontinence - both stress and urgency urinary incontinence. 4. Overflow incontinence - resulting from a hypotonic bladder or bladder outlet obstruction.
56
Identify pharmacological treatments for overactive bladder syndrome.
muscarinic receptor antagonists such as Oxybutinin, Tolterodine, Solifenacin, β3-adrenoceptor agonist Mirabegron.
57
What are the common side effects of muscarinic blockade?
Common side effects of muscarinic blockade include dry mouth, tachycardia, constipation, blurred vision, and urinary retention may occur if there is bladder outflow obstruction. use acronym BCDU
58
treatments for stress incontinence
- pelvic floor exercises - surgery - vaginal oestrogens - duloxetine
59
Define benign prostatic hyperplasia (BPH) and its symptoms.
BPH is a condition in men characterized by bladder outflow obstruction and lower urinary tract symptoms (LUTS), including weak stream and hesitancy. Storage symptoms include urgency, daytime urinary frequency, nocturia, and urinary incontinence. Voiding symptoms include slow stream, splitting or spraying, straining, intermittency, hesitancy, straining, and terminal dribbling. Post-micturition symptoms include post-micturition dribble and the sensation of incomplete emptying.
60
How do you assess the severity of BPH?
The severity of BPH is assessed using the International Prostate Symptom Score (IPSS), which ranges from 0-35.
61
Explain the scoring system of the International Prostate Symptom Score (IPSS).
0-7 indicates mild symptoms, 8-19 indicates moderate symptoms, and 20-35 indicates severe symptoms.
62
first line for LUTS associated with BPH
alpha blockers like doxasozin and tamsulosin
63
What are the potential adverse effects of alpha blockers?
orthostatic hypotension, dizziness, headache, erectile disorders, rhinitis, asthenia, and edema.
64
what other drugs do alpha blcokers usually interact with
other hypotensive agents like calcium channel blockers, beta-blockers, ACE inhibitors, ARBs, and PDE5 inhibitors.
65
What is the first line therapeutic intervention for a patient with a very high IPSS score?
For patients with very high IPSS scores, 5 alpha reductase inhibitors may be considered as a first line therapeutic intervention. finasteride
66
Describe the mechanism of action of 5 alpha reductase inhibitors in BPH.
5 alpha reductase inhibitors work by blocking the conversion of testosterone to dihydrotestosterone (DHT), which reduces prostate size and alleviates symptoms.
67
adverse effects of finasteride
- gynaecomastia - breast tenderness depression - sexual dysfunction (libido, impotence and infertility)
68
Explain the importance of avoiding 5 alpha reductase inhibitors in pregnant women.
Exposure of a male fetus to 5 alpha reductase inhibitors may cause abnormal development of the external genitalia, making it crucial for pregnant women to avoid these drugs.
69
How do gonadotropin-releasing hormone (GnRH) analogues affect hormone levels in prostate cancer treatment?
Chronic administration of GnRH analogues results in sustained suppression of pituitary gonadotropins, leading to serum testosterone levels comparable to surgical castration. initial increase in LH and FSH does occur*
70
example of anti-androgen
flutamide
71
example of gonadorelin analogues
goserelin buserelin
72
Explain the preferred initial approach for systemic therapy in metastatic bladder cancer.
Platinum-based chemotherapy
73
urothelial bladder cancer is most sensitive to
cisplatin based combination chemo
74
what classes of drugs are used in RCC
tyrosine kinase inhibitors = sorafenib + sunitinib mTOR inhibitor = everolimus tyrosine kinase receptor inhibitor = bevacizumab
75
types of oral iron
Ferrous sulfate Ferrous fumarate Ferrous gluconate
76
types of paraenteral iron
Iron dextran Iron sucrose Ferric carboxymaltose Iron isomaltoside 1000
77
What are the common adverse effects associated with oral iron supplementation?
Common adverse effects of oral iron include constipation, diarrhea, epigastric pain, gastrointestinal irritation, and nausea.
78
Explain the importance of timing when taking oral iron in relation to other medications.
Oral iron should be taken at least 2 hours before medications like levothyroxine, bisphosphonates, ciprofloxacin, tetracyclines, calcium, and zinc salts to avoid reduced absorption.
79
Describe the recommended dosing for elemental iron in treating iron deficiency anemia.
The recommended dosing for elemental iron in treating iron deficiency anemia is 65 mg of elemental iron (equivalent to 200 mg of ferrous sulfate) once daily on an empty stomach
80
Postulate a reason for the use of folic acid during pregnancy.
Folic acid is used during pregnancy to help prevent neural tube defects in the developing fetus, as it is crucial for proper cell division and growth.
81
Describe the mechanism of action of folic acid.
Folic acid acts as a coenzyme in the synthesis of nucleic acids and amino acids, which are essential for DNA replication and cell division, thus supporting fetal development.
82
What should be considered when treating macrocytic anemia with suspected Vitamin B12 deficiency?
When treating macrocytic anemia with suspected Vitamin B12 deficiency, it is important to administer vitamin B12 before starting folic acid to prevent the risk of subacute combined degeneration of the cord.
83
Describe the common cause of Vitamin B12 deficiency.
The vast majority of Vitamin B12 deficiency is due to the inability to absorb B12 in the terminal ileum, often caused by a lack of intrinsic factor or conditions like terminal ileal Crohn’s disease.
84
dosages of folate in low risk women
400 micrograms daily before conception and until 12 weeks
85
dosage of folate in high risk women
5mg daily to be taken before conception until week 12