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Year 3 > Block 34 PPT > Flashcards

Block 34 PPT Flashcards

1
Q

AKI - actions?

A
  • Optimise intra-vascular fluid volume - IV fluids
  • Optimise Blood Pressure
  • Withholding drugs that interfere with renal autoregulation (ACEIs, ARBs)
  • Temporary cessation of all drugs that induce hypotension (antihypertensives)
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2
Q

DAMN AKI?

A
  • (diuretics, ACEi/ ARBs, metformin, NSAIDs)
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3
Q

drugs requiring dose reduction or cessation in AKI?

A
  • All medications that are metabolized and excreted by the kidneys should be dose adjusted for an assumed eGFR of < 10 mL/min/1.73m2
  • fractionated heparins
  • opiates
  • penicillin-based antibiotics
  • sulfonylurea-based hypoglycaemic drugs
  • aciclovir
  • metformin
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4
Q

Drugs interfering w renal perfusion?

A
  • ACEi
  • ARBs
  • NSAIDs
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5
Q

drugs requiring close monitoring w renal function?

A
  • warfarin
  • aminoglycosides - gentamicin, tobramycin
  • lithium
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6
Q

drugs aggrevating hyperkalaemia?

A
  • trimethoprim
  • spironolactone
  • amiloride
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7
Q

CKD prescribing?

A
  • The kidneys provide the major route of elimination for water-soluble drugs and water-soluble metabolites
  • Loading doses do not usually require any modification
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8
Q

side effects of gentamicin?

A

*Damage to the cochlear and vestibular apparatus - loss of balance, tinnitus, loss of hearing.
*May cause renal damage - risk of nephrotoxicity is increased with prolonged treatment.

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9
Q

use of gentamicin w ? diuretics increases risk of

A

*Use with ototoxic diuretics, e.g. furosemide, may increase risk of ototoxicity and nephrotoxicity.

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10
Q

gentamicin metabolism?

A
  • given IV
  • hydrophilic - not distrubuted into body fat and minimally disrubted into tissue fluids
  • follows first order kinetics - drug is cleared from blood at a rate proportional to its concentration
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11
Q

gentamicin is excreted unmodified by the ?

A
  • gentamicin is excreted unmodified from the kidneys
  • After a dose, level in the blood decays exponentially.
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12
Q

Acute kidney injury is often preventable by:

A
  • Avoiding nephrotoxic medications where appropriate
  • Ensuring adequate fluid intake (including IV fluids if oral intake is inadequate)
  • Additional fluids before and after radiocontrast agents
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13
Q

Treating AKI involves…

A
  • reversing cause and supportive management
  • e.g. IV fluids for dehydration/ hypovol
  • relive obstruction in post renal - e.g. catheter
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14
Q

Other Tx methods in AKI?

A
  • Withhold medicationsthat mayworsen the condition(e.g., NSAIDs and ACE inhibitors)
  • Withhold/adjust medicationsthat mayaccumulatewith reduced renal function (e.g., metformin and opiates)
  • Dialysismay be required in severe cases
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15
Q

Why do ACEi need to be stopped in AKI?

A
  • ACEi are not nephrotoxic
  • they are stopped in AKI as they reduce filtration pressure
  • but ACEi have a protective effect on the kidneys long term
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16
Q

ACEi are offered to ppts w?

A

HTN, diabetes, CKD to prevent further damage

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17
Q

Most common cause of AKI

A

ATN

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18
Q

What happens in ATN

A
  • Necrosis of renal tubular epithelial cells severely affects the functioning of the kidney.
  • In the early stages ATN is reversible if the cause if removed.
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19
Q

Causes of ATN?

A
  • caused by ischaemia and nephrotoxins: aminoglycosides, radiocontrast agents, lead
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20
Q

Features of ATN?

A
  • features of AKI: raised urea, creatinine, potassium
  • muddy brown casts in the urine
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21
Q

AIN?

A
  • 25% of drug induced AKI
  • drugs: the most common cause, particularly antibiotics
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22
Q

Drugs causing AKI?

A
  • penicillin
  • rifampicin
  • NSAIDs
  • allopurinol
  • furosemide
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23
Q

Treating underlying cause of CKD?

A
  • Optimising diabetic control
  • Optimising hypertension control
  • Reducing or avoiding nephrotoxic drugs
  • Treating glomerulonephritis (where this is the cause)
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24
Q

medications that help slow progression of CKD

A
  • ACE inhibitors(orangiotensin II receptor blockers)
  • SGLT-2 inhibitors(specificallydapagliflozin)
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25
Q

Tx complications of CKD - metabolic acidosis?

A
  • Oralsodium bicarbonate to treat metabolic acidosis
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26
Q

Tx of CKD - anaemia

A

Iron and EPO

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27
Q

treating renal bone disease w CKD?

A
  • Vitamin D,low phosphate dietand phosphate bindersto treatrenal bone disease
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28
Q

Reducing risk of comps from CKD?

A
  • Exercise, maintain a healthy weight and avoid smoking
  • Atorvastatin 20mgfor primary prevention of cardiovascular disease (in all patients with CKD)
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29
Q

role of drugs on progression of CKD?

A

Common nephrotoxic drugs such as certain antibiotics, NSAIDs, contrast agents, and chemotherapeutic agents can accelerate CKD by directly damaging renal cells and exacerbating underlying renal pathology

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30
Q

nephrotoxic drugs?

A

ACE, ARB, calcaeneurin inhibitors, lithium, mesalazine, NSAIDs

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31
Q

Tx of UTI?

A
  • Nitrofurantoin - avoid in renal impairment
  • Trimethoprin - avoid in pregnancy
  • usually 3 days
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32
Q

Avoid nitrofurantoin in ?

A

renal impairment

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33
Q

avoid trimethoprim in?

A

pregnancy

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34
Q

Tx of a complicated UTI?

A
  • oral course of fluoroquinolone
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35
Q

Severe UTI or urosepsis Mx?

A
  • In the presence of more severe disease (e.g. urosepsis) or patients unable to tolerate oral therapy, broad-spectrum IV antibiotics can be used - iV co-amoxiclav or ceftriaxone can be used for urosepsis or acute severe pyelo
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36
Q

uncomplicated pyelonephritis Mx?

A
  • uncomplicated pyelonephritis does not require admission to hospital
  • can be treated w a course of oral fluoroquinolone e.g. ciprofloxacin
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37
Q

complicated pyelo?

A

IV co-amox or ceftriaxone

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38
Q

Altered physiology in renal function?

A
  • impaired renal function affects various processes like filtration, secretion, reabs and metabolism of drugs
  • role of kidneys in eliminating waste and maintaing fluid and electrolyte balance
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39
Q

Pharmacokinetic - dist in RI?

A
  • Distrubution - changes in protein binding due to uremia can affect dist or highly protein bound drugs
  • altered VoD with fluid overload or dehydration
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40
Q

pharmacokinetic - metabolism in RI?

A
  • Metabolism: impaired renal function may lead to decreased drug metabolism, resulting in increased drug levels
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41
Q

Pharmacokinetic - excretion in RI?

A
  • excretion is most sig affected: decreased clearance, longer half lives, increased drug accumulation, inc risk of toxicity
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42
Q

Pharmacodynamic response in RI?

A
  • Increased sensitivity to drugs
  • Toxicity risk espec for renally elimiated drugs
  • nephrotoxic drugs can exacerbate renal dysfunction
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43
Q

Common meds causing harm to patients w impaired renal function?

A
  • Aminoglycosides
  • NSAIDs
  • radiocontrast agents - e.g. iodinated contrast media
  • chemotherapy - cisplatin, methotrexate
  • ACEi/ ARB
  • lithium
  • cyclosporin and tacrolimus
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44
Q

principals involved in selecting medicines and designing dosage regimens for patients with impaired renal function.

A
  • assessment of renal function - eGFR and creatinine clearance
  • drug dose adjustment
  • monitoring
  • avoidance of nephrotoxic drugs
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45
Q

Where to find info about choosing and adjusting drug dosage in impaired renal function ?

A
  • BNF
  • renal drug database
  • NICE CKS
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46
Q

stress incontinence - lifestyle modifications?

A
  • Avoiding caffeine, diuretics and overfilling of the bladder
  • Avoid excessive or restricted fluid intake
  • Weight loss (if appropriate)
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47
Q

3 management options in SI?

A
  • Supervised pelvic floor exercisesfor at least three months before considering surgery
  • Surgery
  • Duloxetineis an SNRI antidepressant used second line where surgery is less preferred
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48
Q

SI - pelvic floor exercises?

A
  • pelvic floor exercises used to strengthen the muscles of the pelvic floor
  • they increase the tone & improve support for the bladder and bowel
  • 8 contractions 3x a day
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49
Q

surgical options for SI?

A
  • Tension free vaginal tape
  • autologous sling procedures
  • colposuspension
  • intramural urethral bulking
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50
Q

TVT?

A
  • Tension-free vaginal tape(TVT) procedures involve a mesh sling looped under the urethra and up behind the pubic symphysis to the abdominal wall. This supports the urethra, reducing stress incontinence.
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51
Q

Autologous sling procedures?

A
  • Autologous sling procedureswork similarly to TVT procedures but a strip of fascia from the patient’s abdominal wallis used rather than tape
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52
Q

colposuspension?

A
  • Colposuspensioninvolves stitches connecting the anterior vaginal wall and the pubic symphysis, around the urethra, pulling the vaginal wall forwards and adding support to the urethra
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53
Q

intramural urethral bulking?

A
  • Intramural urethral bulkinginvolves injections around the urethra to reduce the diameter and add support
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54
Q

management of urge incontinence?

A
  • bladder retraining
  • anticholinergic
  • mirabegron
  • invasive procedures
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55
Q

first line in UI?

A

bladder retraining

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56
Q

bladder retraining?

A
  • Bladder retraining(gradually increasing the time between voiding) for at least six weeks is first-line
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57
Q

UI - anticholinergics?

A
  • Anticholinergic medication, for example, oxybutynin, tolterodine and solifenacin
  • Mirabegron is an alternative to anticholinergic medications
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58
Q

SE of anticholinergic?

A
  • anticholinergic SEs: dry mouth, dry eyes, urinary retention, constipation, postural hypotension
  • can lead to cognitive decline, memory problems and worsening of dementia
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59
Q

Invasive options for overactive bladder that has failed to respond to retraining and medical management include:

A
  • Botulinum toxin type Ainjectioninto the bladder wall
  • Percutaneous sacral nerve stimulationinvolves implanting a device in the back that stimulates the sacral nerves
  • Augmentation cystoplastyinvolves using bowel tissue to enlarge the bladder
  • Urinary diversioninvolves redirecting urinary flow to a urostomy on the abdomen
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60
Q

Mx of mixed incontinence?

A
  • target treatment at the type that appears to most contribute to the symptoms
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61
Q

overactive bladder Tx?

A
  • bladder training
  • if symptoms persist, consider adding an antimuscarinic like oxybutynin first line
  • Mirabegron — if an antimuscarinic drug is contraindicated
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62
Q

overactive bladder in a post menopausal woman?

A
  • if the woman is post-menopausal and has vaginal atrophy consider intravaginal oestrogen therapy
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63
Q

Overactive bladder - troublesome noctura?

A

desmopressin

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64
Q

OB - secondary care?

A
  • Treatment options in secondary care include injection of botulinum toxin type Ainto the bladder wall, percutaneous sacral nerve stimulation, augmentation cystoplasty, and urinary diversion.
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65
Q

BPH and LUTS drug options?

A
  • alpha blockers
  • 5-AR
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66
Q

Alpha blockers?

A
  • Alpha-blockers(e.g.,tamsulosin) relax smooth muscle, with rapidimprovement in symptoms
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67
Q

5-AR inhibitors?

A
  • 5-alpha reductase inhibitors(e.g.,finasteride) gradually reduce thesize of the prostate
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68
Q

how do 5-AR inhibitors work?

A
  • 5 alpha reductase converts testosterone to dihydrotestosterone (DHT), which is a more potentandrogen hormone. Inhibitors of 5-alpha reductase (i.e. finasteride) reduce DHT in the tissues, including the prostate, leading to a reduction in prostate size.
  • It takes up to 6 months of treatment for the effects to result in an improvement in symptoms.
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69
Q

surgical options for BPH/ LUTS?

A
  • Transurethral resection of the prostate(TURP)
  • Transurethral electrovaporisation of the prostate(TEVAP/TUVP)
  • Holmium laser enucleation of the prostate(HoLEP)
  • Open prostatectomyvia an abdominal or perineal incision
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70
Q

conservative measures of LUTS/ BPH?

A
  • pelvic floor muscle training
  • bladder training
  • prudent fluid intake
  • containment products
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71
Q

Mx of bladder cancer?

A
  • TURBT
  • intravesical chemo
  • intravesical BCG
  • radical cystectomy
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72
Q

TURBT?

A
  • Transurethral resection of bladder tumour(TURBT) may be used for non-muscle-invasive bladder cancer. The involves removing the bladder tumour during a cystoscopy procedure.
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73
Q

BC - intravesical chemo?

A
  • Intravesical chemotherapy(chemotherapy given into the bladder through a catheter) is often used after a TURBT procedure to reduce the risk of recurrence.
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74
Q

intravesical BCG?

A
  • Intravesical Bacillus Calmette-Guérin (BCG)may be used as a form of immunotherapy. Giving theBCG vaccine(the same one as for tuberculosis) into the bladder is thought to stimulate the immune system, which in turn attacks the bladder tumours.
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75
Q

Radical cystectomy ?

A
  • Radical cystectomyinvolves the removal of the entire bladder. Following removal of the bladder, there are several options for draining urine:
  • Urostomy with an ileal conduit (most common)
  • Continent urinary diversion
  • Neobladder reconstruction
  • Ureterosigmoidostomy
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76
Q

chemotherapy in BC?

A
  • Chemotherapy like cistplatinandradiotherapymay also be used.
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77
Q

RCC first line

A
  • surgery is first line - partial or radical nephrectomy
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78
Q

RCC - Where patients are not suitable for surgery, less invasive procedures can be used to treat the cancer:

A
  • arterial embolisation
  • perc cryotherapy
  • radiofreq ablation
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79
Q

arterial embolisation?

A

cutting off the blood supply to the affected kidney

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80
Q

percutaneous cryotherapy?

A

injecting liquid nitrogen to freeze and kill the tumour cells

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81
Q

radiofreq ablation?

A
  • Radiofrequency ablation, putting a needle in the tumour and using an electrical current to kill the tumour cells
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82
Q

advanced RCC mx?

A

TKI and mTOR

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83
Q

TKI e.g.

A

sunitinib

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84
Q

mTOR?

A
  • Temsirolimus/ everolimus: inhibitor of the mammalian target of rapamycin (mTOR)
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85
Q

Mx of prostate cancer?

A
  • Surveillanceorwatchful waitingin early prostate cancer
  • External beam radiotherapydirected at the prostate
  • Brachytherapy
  • Hormone therapy
  • Surgery
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86
Q

EBR key side effect?

A
  • Proctitis is a key side effect
  • caused by radiation affecting the rectum
  • Proctitis can cause pain, altered bowel habit, rectal bleeding and discharge
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87
Q

bracytherapy for PC?

A
  • involves implanting radioactive metal “seeds” into the prostate.
  • This delivers continuous, targeted radiotherapy to the prostate.
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88
Q

Side effect of bracytherapy?

A
  • can cause cystitis and proctitis, ED, incontinence
  • increased risk or bladder or rectal cancer
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89
Q

hormone therapy for PC?

A
  • aims to reduce levels of androgens :
  • Androgen-receptor blockerssuch as bicalutamide, Cyproterone acetate
  • GnRH agonistssuch as goserelin(Zoladex) orleuprorelin(Prostap)
  • Bilateral orchidectomyto remove the testicles (rarely used)
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90
Q

Side effects of hormone therapy for PC?

A
  • Hot flushes
  • Sexual dysfunction
  • Gynaecomastia
  • Fatigue
  • Osteoporosis
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91
Q

Radical prostatectomy

A
  • removal of entire prostate
  • key comps: ED, UI
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92
Q

Modifiable RF for ED?

A
  • Smoking cessation
  • minimal alcohol intake
  • weight loss
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93
Q

psychosexual counselling for ED?

A
  • if there’s a psychogenic component and if purely organic causes have been ruled out
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94
Q

drug classes for ED?

A
  • PDE-5 inhib like slidenafil
  • PE-1 analogue - aprostadil
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95
Q

PDE-5 inhibitors?

A
  • These drugs arrest PDE-5, allowing for the prolongation of cGMP and subsequent relaxation of penile blood vessels (sildenafil, vardenafil, avanafil).
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96
Q

PE-1 analogues?

A
  • Alprostadil
  • induces vascular SM relaxation
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97
Q

penile prosthesis?

A
  • recommended when previous treatments have failed
  • inflatable implants vs semirigid rods
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98
Q

new IDA without an underlying cause?

A

New iron deficiency in an adult without a clear underlying cause (e.g., heavy menstruation or pregnancy) should be investigated further, including acolonoscopyandoesophagogastroduodenoscopy(OGD) for malignancy.

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99
Q

Three options for treating IDA?

A
  • Oral iron
  • iron infusion
  • blood tranfusion
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100
Q

Oral iron?

A
  • Oral iron(e.g., ferrous sulphate or ferrous fumarate)
  • side effects: constipation and black stools
  • need to be taken for 3 months after levels have been corrected
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101
Q

iron infusion?

A
  • Iron infusion(e.g., IV CosmoFer)
  • rapid boost
  • small risk of allergic reactions
  • avoided in infections - risk of feeding bacteria
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102
Q

iron rich diet?

A
  • Iron-rich diet: this includes dark-green leafy vegetables, meat, iron-fortified bread
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103
Q

B12 def Mx?

A
  • IM hydroxocobalamin
  • in patients with co-existing folate deficiency, B12must be replaced first as folate replacement in this setting may precipitate neurological complications (e.g. subacute degeneration of the cord).
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104
Q

B12 > B9 replacement because

A

risk of subacute degeneration of the cord

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105
Q

foods rich in b12?

A
  • Eggs.
  • Foods which have been fortified with vitamin B12 (for example some soy products, and some breakfast cereals and breads) are good alternative sources to meat, eggs, and dairy products.
  • Meat.
  • Milk and other dairy products.
  • Salmon and cod.
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106
Q

Folate def?

A
  • folic acid supplementation
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107
Q

sources of folate?

A
  • Asparagus.
  • Broccoli.
  • Brown rice.
  • Brussels sprouts.
  • Chickpeas.
  • Peas.
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108
Q

packed red cells indications?

A
  • Indicated for patients with symptomatic anemia, acute blood loss, or impaired oxygen delivery.
  • Major haemorrhage
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109
Q

FFP is used for?

A
  • Used to correct coagulation factor deficiencies in patients with bleeding disorders or massive transfusions.
  • clinically sig bleeding but without major haemorrhage if they have an coagulation results
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110
Q

platelet concentrates are used for?

A
  • Administered to patients with thrombocytopenia or platelet dysfunction to prevent or treat bleeding.
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111
Q

cryoprecipitate Ix?

A
  • Contains high concentrations of fibrinogen, factor VIII, and von Willebrand factor, used in cases of hypofibrinogenemia or von Willebrand disease.
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112
Q

albumin is used for?

A
  • Used for volume expansion and to maintain colloid osmotic pressure in patients with hypoalbuminemia or hypovolemia.
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113
Q

factor concentrayes Ix?

A
  • Specific coagulation factors (e.g., factor VIII for hemophilia A) administered to patients with congenital or acquired clotting factor deficiencies.
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114
Q

granulocytes concentrates Ix?

A
  • Utilized in patients with severe neutropenia or neutrophil dysfunction to prevent or treat infections.
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115
Q

immunoglobulins Ix?

A
  • Administered for passive immunity in patients with immunodeficiencies or autoimmune disorders.
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116
Q

whole blood transfusions?

A
  • Used in specific clinical scenarios, such as massive transfusion protocols or exchange transfusions.
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117
Q

Prothrombin complex concentrate is used immediately for?

A
  • offer immediate prothrombin complex concentrate transfusions for the emergency reversal of warfarin AC in ppts w either
  • severe bleeding
  • or head injury with suspected inracerebral haemorrhage
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118
Q

Mx of hypothyroidism?

A
  • levothyroxine: synthetic T4 which is metabolised to T3 in the body
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119
Q

Mx of hyperthyroidism - whilst decision on definitive therapy is being made?

A
  • thionamides - carbimazole or propylthiouracil whilst decision on definitive therpay is being made
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120
Q

definitie Mx of hyperthyroidism?

A
  • definitive therapy = radioactive iodine, ongoing thionamide therapy or surgery
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121
Q

symptomatic treatment of hyperthyroidism?

A
  • BB or CCB can be prescribed to reduce adrenergic symptoms whilst thionamides take effect
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122
Q

radioactive iodine therapy?

A
  • taken up by the thyroid causing destruction and reduced thyroid hormone release
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123
Q

thionamides?

A
  • carbimazole first line
  • teratogenic - especially in T1
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124
Q

when is PTU considered?

A
  • Intolerant/allergic to carbimazole
  • Pregnant or planning on pregnancy in the next 6 months
  • A history of pancreatitis
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125
Q

testing before thionamide tx?

A
  • Baseline FBC and LFTs are obtained prior to the commencement of thioamides.
  • Neutropenia or severely deranged transaminases are a contraindication to treatment.
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126
Q

severe side effects of thionamides?

A
  • Agranulocytosis is a severe side effect associated with both thioamides
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127
Q

thyroidectomy?

A
  • may be used as definitive therapy if malignancy is suspected, there is a compressive goitre or RAI/ anti-thyroid medications are unsuitable.
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128
Q

hemithyroidectomy?

A
  • Hemithyroidectomy (removal of half the thyroid gland) may be offered to patients with a solitary toxic nodule.
129
Q

complications of thyroidectomy?

A

hypocalcaemia, recurrent LN injury

130
Q

AP hormones?

A
  • ACTH
  • FSH, LH
  • gh
131
Q

testing adrenal function in panhypopituitarism - ACTH?

A
  • Tetracosactide(tetracosactrin), an analogue of corticotropin (ACTH), is used to test adrenocortical function
  • failure of the plasma cortisol concentration to rise after administration oftetracosactideindicates adrenal insufficiency
132
Q

Replacing gonadotrophin function in panhypopituitarism?

A
  • FSH + LH used in the treatment of infertility in women with proven hypopituitarism or who have not responded toclomifene citrate
133
Q

GH indications?

A
  • In children it is used in Prader-Willi syndrome, Turner syndrome, chronic renal insufficiency, short children considered small for gestational age at birth, and short stature homeobox-containing gene (SHOX) deficiency
  • somatropin
134
Q

hypothalamic hormone replacement?

A
  • gonadorelin leads to rapid rise in LH and FSH
  • Gonadorelin analoguesare indicated in endometriosis and infertility and in breast and prostate cancer.
135
Q

Mx of hyperprolactinaemia?

A
  • bromocriptine used for treatment of galactorrhoea and treatment of prolactinomas
  • cabergolline
136
Q

suppression of lactation - if DRA is required,

A
  • if DRA is req, cabergoline is preferred to bromocriptine
137
Q

Mx of hypogonadism?

A
  • Address any reversible factors contributing to hypogonadism, such as lifestyle modifications (weight loss, smoking cessation), treatment of underlying conditions (e.g., obesity, diabetes), or removal of medications causing hypogonadism
  • Testosterone replacement therapy
138
Q

when is GH therapy recommended?

A
  • proven growth hormone deficiency
  • Turner’s syndrome
  • Prader-Willi syndrome
  • chronic renal insufficiency before puberty
139
Q

GH replacement is given by?

A
  • given by subcutaneous injection
  • GH replacement - recombinant human GH before bed - somatotropin
140
Q

drugs in chronic adrenal insufficiency?

A
  • Glucocorticoid replacement - hydrocortisone
  • Mineralcorticoid replacement - fludrocostisone
  • Androgen replacement - DHEA replacement in women
141
Q

AI - 3 drugs

A

hydrocortisone, fludorcortisone, DHEA (in women)

142
Q

steroids in CAI?

A
  • ppts given a steroid card, ID tag and emergency letter to alert that they depend on steroids
  • Doses are doubledduring an acute illness to match the normal steroid response to illness.
143
Q

Addisonian crisis Mx?

A
  • Intensive monitoringif they are acutely unwell
  • Parenteral steroids (i.e.IV hydrocortisone)
  • IV fluidresuscitation
  • Correct hypoglycaemia
  • Careful monitoring of electrolytes and fluid balance
144
Q

summary of drugs in addisonian crisis?

A
  • IV hydrocortisone
  • IV fluids
145
Q

initial Mx of hypercal?

A

rehydration w normal saline

146
Q

what can be done in hypercal after the ppt has been rehydrated?

A
  • bisphosphonates
  • calcitonin - quicker than bisphosphonates
  • steroids in sarcoidosis
147
Q

? are sometimes used in hypercal, paticularly in ppts who can’t tolerate aggressive fluids?

A
  • Loop diuretics such as furosemide are sometimes used in hypercalcaemia, particularly in patients who cannot tolerate aggressive fluid rehydration.
148
Q

surgery in hyperclacemia?

A
  • surgery: able to provide a cure in primary hyperparathyroidism. Potential option in tertiary hyperparathyroidism
149
Q

dialysis in hypercal?

A

reserved for severe, refractory hypercalcaemia.

150
Q

Hypercalcaemia -Mild (< 3 mmol/L) and asymptomatic/mild symptoms:

A

increase oral fluids and avoid precipitants (e.g. thiazide diuretics, lithium, dehydration).

151
Q

moderate hypercal (3-3.5)?

A

acute rise requires inpatient admission for intravenous fluids. Chronically raised elevations may not require acute management depending on the aetiology and symptomatology.

152
Q

severe hypercal - 3.5?

A

all patients require urgent admission to hospital and treatment. Treatment involves aggressive intravenous fluids and consideration of bisphosphonates, particularly if malignancy is suspected.

153
Q

management of an adult patient withhypocalcaemia/vitamin D deficiency/(osteomalacia).

A
  • colecalciferol(vitamin D₃).
154
Q

NICE recommends checking calcium level within a month of the loading regime for osteomalacia:

A
  • Low incalcium deficiency
  • High inprimary hyperparathyroidism(previously masked by the vitamin D deficiency)
  • High in other conditions that cause hypercalcaemia, such ascancer,sarcoidosisortuberculosis
155
Q

RF for osteopososis?

A
  • address reversible RF - physical activity, maintain healthy weight, stop smoking, reduce alcohol consumption
  • address calcium and vitamin D intake
156
Q

bisphosphonates ?

A
  • first line Tx of osteoporosis
  • considered in ppts on long term steroids
157
Q

Bisphosphonateshave some important side effects:

A
  • Refluxandoesophageal erosions
  • Atypical fractures(e.g., atypical femoral fractures)
  • Osteonecrosisof thejaw(regular dental checkups are recommended before and during treatment)
  • Osteonecrosisof theexternal auditory canal
158
Q

how should bisphosphonates be taken?

A

Oral bisphosphonatesare taken on anempty stomachwith a full glass of water. Afterwards, the patient shouldsit uprightfor 30 minutes before moving or eating to reduce the risk ofrefluxandoesophageal erosions.

159
Q

other Tx of osteoporosis?

A
  • denosumab
  • romosozumab
  • teriparatode
  • HRT
  • raloxifene
160
Q

denosumab?

A

monoclonal antibody that targets osteoclasts)

161
Q

romosozumab?

A
  • Romosozumab(a monoclonal antibody that targets sclerostin – a protein in osteocytes that inhibits bone formation)
162
Q

teriparatide?

A
  • Teriparatide(acts as parathyroid hormone)
163
Q

HRT?

A

used for osteoporosis paricularly in women w early meno

164
Q

Raloxifene?

A

SERM

165
Q

Hyponatraemia - hypervolaemic cause?

A
  • normal, i.e. isotonic, saline (0.9% NaCl)
  • this may sometimes be given as a trial
  • if the serum sodium rises this supports a diagnosis of hypovolemic hyponatraemia
  • if the serum sodium falls an alternative diagnosis such as SIADH is likely
166
Q

euvolemic hyponatreamia - most common cause?

A

SIADH

167
Q

Euvolemic hyponatreamia Mx?

A
  • fluid restrictto 500-1000 mL/day
  • demeclocycline - ADH inhibitor
  • vaptans - vasopressin receptor antagonist
168
Q

hypervolaemic hyponatreamia?

A
  • fluid restrictto 500-1000 mL/day
  • consider loop diuretics
  • consider vaptans
169
Q

what are vaptans?

A
  • ADH antagonists
  • act on V2 receptors, resulting in selective water diuresis, sparing electrolytes
170
Q

vaptans should be avoided in?

A

should be avoided in ppts who have hypovolaemic hyponatreamia

171
Q

Severe hyponatreamic can result in?

A
  • untreated severe hyponatreamia may result in cerebral oedema which can cause brain herniation
172
Q

acute hyponatreamia management?

A
  • acute hyponatraemia - Hypertonic saline (typically 3% NaCl)is used to correct the sodium level more quickly than would be done in patients with chronic hyponatraemia
173
Q

acute hyponatreamia should be managed in?

A

high dependency unit (HDU) espec if neurological symptoms are present

174
Q

DI - underlying cause?

A

The underlying cause should be treated (e.g., stopping lithium). Mild cases may be managed conservatively.

175
Q

Cranial diabetes insipidus Mx?

A
  • desmopressin - synthetic ADH to replace missing ADH
  • serum sodium needs to be monitored, as there is a risk ofhyponatraemia(low sodium) with desmopressin.
176
Q

Nephrogenic diabetes insipidusmanagement options include:

A
  • Ensuring access to plenty of water
  • High-dose desmopressin
  • Thiazide diuretics
  • NSAIDs
177
Q

urge incont associated w

A

OBS

178
Q

stress incont due to?

A

urethral sphincter incompetence.

179
Q

Overflow incontinence with continuous urine leakage from

A

hypotonic bladder or bladder outlet obstruction producing urinary retention

180
Q

drugs for urinary urgency?

A
  • Muscarinic antagonists: oxybutinin, tolerodine
  • B-3 receptor agonists: mirabegron
181
Q

muscarinic blockage side effects?

A
  • BCDU
  • dry mouth
  • tachy
  • constipation
  • bludder vision
  • urinary retention if there’s bladder outflow obst
182
Q

Drug interactions ofr alpha blockers?

A
  • Mostly by pharmacodynamic interaction causing hypotension
  • Other hypotensive agents
  • CCBs
  • Beta – blockers
  • ACE Is, ARBs
  • PDE 5 inhibitors - Sildenafil & Vardenafil
183
Q

5-AR inhibitors absolute contra-indication?

A

Exposure of a male fetus to 5α-reductase inhibitors may cause abnormal development of the external genitalia. It is therefore important that pregnant womendo not take these drugs and are not exposed to them, e.g. by handling broken or damaged tablets or through semen during unprotected sex with a man taking these drugs.

184
Q

side effects of 5-ARi like finasteride?

A
  • Breast enlargement
  • Breast tenderness
  • Decreased libido
  • Ejaculation disorders
  • Impotence
185
Q

BC - cisplatin based chemo?

A
  • Urothelial bladder cancer is most sensitive to cisplatin-based combination chemotherapy
186
Q

platininum based chemo in BC?

A
  • Platinum-based chemotherapy is the preferred initial approach for systemic therapy in patients with metastatic disease.
187
Q

drug interaction of iron salts

A
  • Mostly by reducing absorption
  • Levothyroxine
  • Bisphosphonates
  • Ciprofloxacin
  • Tetracyclines
  • Calcium and zinc salts
  • These medications should therefore be taken at least 2 hours before oraliron.
188
Q

Ooral dose of iron for IDA?

A
  • oral dose of elemental iron for IDA should be 100 to 200mg daily
189
Q

B12 replacement

A
  • If treating a macrocytic anaemia where there may be a suspected Vitamin B12 deficiency (i.e. you don’t know the serum B12 levels are absolutely and categorically normal) – always give vitamin B12 before starting folic acid.
  • Risk of subacute combined degeneration of the cord
190
Q

majority of b12 deficiency is caused by?

A
  • The vast majority of vitamin B12 deficiency is due to inability to absorb B12 in the terminal ileum (e.g. lack of intrinsic factor, terminal ileal Crohn’s disease)
191
Q

non pharm management of T2 diabetes?

A
  • lifestyle advice
  • dietary changes, exercise and physical activity, alcohol consumption and smoking cessation
  • especially for pre diabetes - 42-47mmol
192
Q

Diet for T2D?

A
  • Patients should be encouraged to maintain a healthy balanced diet with plenty of fibre, low-index carbohydrate and controlling the intake of high-fat foods
193
Q

T2D should avoid?

A
  • Alcohol increases weight and may exacerbate or prolong hypoglycaemia induced by antidiabetic medications.
194
Q

step 1 in the management of T2D?

A
  • Standard release metformin
  • Aim for HbA1c < 48 mmol/mol, increasing dose as needed
195
Q

monitoring w metformin?

A
  • Monitor renal function, consider modified-release preparations if develop adverse GI effects
196
Q

step 2 in T2D Mx?

A
  • Consider dual antidiabetic therapy if HbA1c rises > 58 mmol/L
  • Metformin in combination with a second antidiabetic agent:
  • Sulfonylurea (SU)
  • Dipeptidyl peptidase-4 inhibitor (DPP-4i)
  • Pioglitazone
  • Sodium–glucose cotransporter 2 inhibitor (SGLT-2i)
197
Q

HbA1c aim for dual antidiabetic therapy?

A

less than 53 mmol

198
Q

diabetes management summary?

A

1) metformin
2) metformin + second agent
3) metformin + 2 agents or insulin based regime
4) metformin, SU, GLP-1, insulin

199
Q

When should triple antidiabtic therapy be considered?

A

Consider triple antidiabetic therapy or an insulin-based regimen if HbA1c > 58 mmol/

200
Q

step 3: triple antidiabetic therapy?

A
  • Metformin, DPP-4i and SU
  • Metformin, pioglitazone and SU
  • Metformin, pioglitazone/SU, and SGLT-2i
201
Q

step 4 in diabetes Mx?

A
  • consider combination treatment with metformin, SU, GLP-1 analogue (if criteria for GLP-1 met)
  • insulin
202
Q

Step 1 of D managemenrt when metformin CI?

A
  • DPP-4i or pioglitazone or SU
  • Aim for HbA1c < 48 mmol/mol or < 53 mmol/mol if treatment with a SU
203
Q

Step 2 when metformin CI?

A
  • If HbA1c rises > 58 mmol/mol consider a combination of:
  • SU and pioglitazone
  • SU and DPP-4i or
  • Pioglitazone and DPP-4i
204
Q

Step 3 when metformin CI

A
  • consider insulin if >58
205
Q

tX aims in diabetes

A
  • Management with lifestyle modifications only: aim HbA1c < 48 mmol/mol
  • Management with lifestyle and a single antidiabetic agent: aim HbA1c < 48 mmol/mol
  • Management with a drug associated with hypoglycaemia (e.g. SU): aim HbA1c < 53 mmol/mol
  • Management with higher intensification regimes: aim HbA1c < 53 mmol/mol
206
Q

insulin in T2D?

A
  • considered when there is poor glycaemic control despite dual AP therapy
  • may not be appropriate when: risk of hypos, concerns relating to licensing for driving gr 2 vehicles, can exacerbate weight loss
207
Q

which type of insulin is offered to T2D?

A
  • patients are offered an intermediate-acting insulin therapy such as NPH in the initial stages.
208
Q

insulin used when hba1c is v high in T2D?

A
  • If glycemic control is particularly bad (e.g. HbA1c > 75 mmol/L) patients may be started on mixed insulin (intermediate and short-acting).
209
Q

long acting insulin in T2D?

A
  • Long-acting insulin is usually reserved for patients where hypoglycaemia is a problem with NPH insulin or the patients rely on carers for help with their injections
210
Q

First line in T2D summar

A
211
Q

When should SFLT2 inhibioy be given?

A
  • should be given in addition to metformin if:
  • high risk of CVD e.g. QRISK >10%
  • established cvd
  • CHF
  • SGLT-2 inhibitors should also be started at any point if a patient develops CVD (e.g. is diagnosed with ischaemic heart disease), a QRISK ≥ 10% or chronic heart failure
212
Q

when SGLT2 and metformin are being used,

A
  • metformin should be established and titrated up before introducing the SGLT-2 inhibitor
213
Q

further Mx of T2D?

A
214
Q

if SGLT2 required but metformin is CI?

A
  • if the patient has a risk of CVD, established CVD or chronic heart failure:
  • SGLT-2 monotherapy
215
Q

If metformin is CI and there is no risk of CVD or HF?

A
  • DPP€‘4 inhibitor or pioglitazone or a sulfonylurea
216
Q

Tx of HTN in diabetes?

A
  • Same as for ppts without T2D
  • ACEi first line in whites
  • ARB first line in blacks
217
Q

Lipid modification in diabetes?

A
  • atorvasatin if QRISK >10%
218
Q

BG monitoring in T1D?

A
  • At least 4x a day including before each meal and before bedM
219
Q

When is more freq blood glucose monitoring required?

A
  • more frequent monitoring is recommended if frequency of hypoglycaemic episodes increases; during periods of illness; before, during and after sport; when planning pregnancy, during pregnancy and while breastfeeding
220
Q

first line insulin therapy in T1D?

A
  • 1) multiple injection basal bolus regime which involves background long acting insulin and short acting insulin injected 30 mins before carbs
221
Q

and what doe s it require

insulin pumps?

A
  • Insulin pumps - constant infusion - alt to basal bolus regimes
  • pump pushes insulin through a cannula which is replaced every 2-3 days to prevent lipodystophy
222
Q

tethered pumps?

A
  • Tethered pumpsare devices with replaceable infusion sets and insulin. They are usually attached to the patient’s belt or around the waist with a tube connecting the pump to the insertion site. The controls for the infusion are on the pump itself.
223
Q

patch insulin pumps?

A
  • Patch pumpssit directly on the skin without any visible tubes. When they run out of insulin, the entire patch pump is disposed of, and a new pump is attached. A separate remote usually controls patch pumps.
224
Q

One, two, or three injections per day insulin regime?

A
  • One, two, or three injections per day regime:traditionally a biphasic regime with the use of both short-acting and intermediate-acting insulin as separate injections or a mixed product.
225
Q

what are the short acting insulins?

A
  • Actrapid and Humulin S are short acting human insulins.
  • Humalog, Novorapid and Apidra are short acting analogue insulins.
226
Q

main principles of DKA managements?

A
  • fluid replacement - isotonic saline
  • insulin - IV infusion
  • glucose - add when less than 14
227
Q

electrolyte abn in DKA?

A
  • correction of electrolyte abn - potassium often falls quickly following treatment with insulin -> hypokalaemia
228
Q

Which type of insulin should be continued in DKA?

A

long acting continued, short acting stopped

229
Q

DKA - slower infusion in?

A
  • slower infusion for young adults (18-25) -> risk of cerebral oedema
230
Q

DKA resolution is defined as:

A
  • pH >7.3 and
  • blood ketones < 0.6 mmol/L and
  • bicarbonate > 15.0mmol/L
231
Q

The goals of management of HHS can be summarised as follows:

A
    1. Normalise the osmolality (gradually)
    1. Replace fluid and electrolyte losses
    1. Normalise blood glucose (gradually)
232
Q

first line in HHS?

A

fluid replacement - 0.9% NaCl

233
Q

Fluid replacement in HHS?

A
  • The aim of treatment should be to replace approximately 50% of estimated fluid loss within the first 12 hours and the remainder in the following 12 hours
  • Fluid replacement alone (without insulin) will gradually lower blood glucose which will reduce osmolality
  • rapid changes need to be avoided
234
Q

insulin in HHS?

A
  • sig ketoneaemia -> give insulin otherwise do NOT
235
Q

mechanism of insulin in HHS?

A
  • Because most patients with HHS are insulin sensitive (e.g. it usually occurs in T2DM), administration of insulin can result in a rapid decline of serum glucose and thus osmolarity.
  • Insulin treatment prior to adequate fluid replacement may result in cardiovascular collapse as the water moves out of the intravascular space, with a resulting decline in intravascular volume.
  • A steep decline in serum osmolarity may also precipitate CPM.
236
Q

Electroyte that needs to be corrected w HHS?

A

k+

237
Q

Potassium shifts in HHS?

A
  • Patients with HHS are potassium deplete but less acidotic than those with DKA so potassium shifts are less pronounced
  • Hyperkalaemia can be present with acute kidney injury
  • Patients on diuretics may be profoundly hypokalaemic
238
Q

Management of hypoglycaemia in the community (for example, diabetes mellitus patients who inject insulin):

A
  • Initially, oral glucose 10-20g should be given in liquid form or sugar lumps.
  • Alternatively, a propriety quick-acting carbohydrate may be given: GlucoGel or Dextrogel
  • A ‘HypoKit’ may be prescribed which contains a syringe and vial of glucagon for IM or SC injection at home
239
Q

Management of hypoglycaemia in hosp

A
  • If the patient is alert, a quick-acting carbohydrate may be given .
  • If the patient is unconscious or unable to swallow, subcutaneous or intramuscular injection glucagon may be given.
  • Alternatively, intravenous 20% glucose solution may be given through a large vein
240
Q

Insulin

perioperative care in diabetics - day surgery

A
  • day surgery may only need reduction in insulin dose or omission/continuation of oral drug
  • Use of variable rate insulin infusion + Glucose
  • Transition back to usual diabetes regimen
241
Q

Elective surgery - minor procedures in patients w good glycaemic control

A
  • HbA1c less than 69 who are undergoing minor procedures can usually be managed by adjusting their insulin regimen
  • On the day before the surgery, the patient’s usual insulin should be given as normal, other than once daily long-acting insulin analogues, which should be given at a dose reduced by 20%.
242
Q

Elective surgery—major procedures or poor glycaemic control?

A
  • major procedures (longer fasting period of more than one missed meal) or poor diabetes control -> variable rate IV insulin infusion
  • continued until the patient is eating/drinking and stabilised on their previous glucose-lowering medication
243
Q

insulin use in major procedures or poor fglycaemic control?

A
  • long acting insulin should be given at 80% of the normal dose the day before and day of, all other insulin should be stopped until their eating and drinking again
244
Q

major procedures/ poor glycaemic control - on the day of surgery give?

A
  • on the day of surgery, start IV infusion of KCl - To prevent hypoglycaemia, this infusion mustnotbe stopped while the insulin infusion is running
  • variable rate IV infusion of insulin in sodium chloride should be gviven at intiial infusion
245
Q

Which diabetes meds can be taken as normal during the whole periop period?

A
  • Pioglitazone, gliptins, GLP-1 analogues can be taken as normal during the whole perioperative period
246
Q

what should be omitted on the day of surgery?

A
  • SGLT-2 inhibitors should be omitted on the day of surgery - their use during periods of dehydration and acute illness is associated with an increased risk of developing diabetic ketoacidosis.
247
Q

which drug is associated w hypo in the fasted state and needs to be omitted the day of surgery?

A
  • sulfonylureas - associated w hypo in the fasted state and so should always be omitted the day of surgery until eating and drinking
248
Q

which drug can be cont unless the patient cwill miss more than1 meal?

A
  • Metformin - can be continued less the patient will miss more than one meal or sig risk of AKI -> lactic acidosis
249
Q

SGLT2 inhibitors are associated w ?

A

inc risk of developing DKA during dehydration, stress, surgery. trauma, acute ilness or other catabolic states

250
Q

diabetes drugs and surgery summary table

A
251
Q

Sick day rules - type 1?

A
  • patient cannot stop insulin due to risk of DKA
  • more freq glucose monitoring
  • maintain normal meal pattern or replace meals w carb drinks
  • 3L of fluid to prevent dehydration
252
Q

sick day in type 2 duabetcs?

A
  • advise the patient to temporarily stop some oral hypoglycaemics during an acute illness
  • medication may be restarted once the person is feeling better and eating and drinking for 24-48 hours
253
Q

sick day - metformin?

A
  • metformin: stop treatment if there is a risk of dehydration, to reduce the risk of lactic acidosis
254
Q

Diabetes sick day - sulfonylureas?

A

increase the risk of hypoglycaemia

255
Q

diabetes sick day rules - SGLT2 INHIB?

A
  • SGLT-2 inhibitors: check for ketones and stop treatment if acutely unwell and/or at risk of dehydration, due to the risk of euglycaemic DKA
256
Q

Diabetes sick day rules - GLP-1 agonists?

A
  • GLP-1 receptor agonists: stop treatment if there is a risk of dehydration, to reduce the risk of AKI
257
Q

Diabetes sick day - insulin?

A
  • if on insulin therapy, do not stop treatment
  • monitor blood glucose more frequently as necessary
258
Q

rapid acting insulin?

A
  • Novorapid, humalog, apidra
  • dec risk of hypoglycaemia
259
Q

short acting insulin?

A
  • soluble
  • actrapid, humulin S
  • slower onset and longer duration
260
Q

Insulin - multiple daily injections?

A

*Most T1DM

261
Q

Biphasic insulin twice daily?

A

*T2DM
*T1DM incapable of using MDI

262
Q

When is it used

long acting once daily insulin?

A

*T2DM usually with oral drugs

263
Q

Continuous subcutaneous insulin infusion (CSII)

A

*T1DM

264
Q

DAFNE?

A

DAFNE stands for Dose Adjustment for Normal Eating. It’s an educational program for people with type 1 diabetes aimed at helping them better manage their condition through understanding the effects of food, insulin, and exercise on blood sugar levels. DAFNE teaches individuals how to adjust their insulin doses based on factors like carbohydrate intake, physical activity, and blood glucose levels to achieve better control over their diabetes

265
Q

Summary of diabetes meds

A
266
Q

summary of further insulin Tx ?

A
267
Q

metformin and renal activity?

A
  • 100% renal clearance - can’t use in RI
  • decreases gluconeogesis and increases peripheral insulin sensitivity
268
Q

sulfonylreas SE?

A
  • weight gain
  • GI side effects
  • can cause hypoglycaemia!!
269
Q

pioglitazone (thiazolindinediones)?

A
  • weight gain
  • edema
  • heart failure - espc when given w insulin
  • Small bone fractures (esp women)
  • Small increased risk of bladder cancer
270
Q

Pioglitazone and insulin ->

A

HF

271
Q

ddp4 inhib SE?

A
  • No hypoglycaemia as monotherapy
  • Weight neutral
  • Low potency
272
Q

Which DDP4 inhibitors need dose adjustemtn for renal impairment?

A
  • Sitagliptin and saxagliptin need dose adjustment for renal impairment
273
Q

which DDP4i doesnt need dose adjustemnt for RI?

A
  • Linagliptin no need for renal dose adjustment
274
Q

SGLT2 impact on weight?

A
  • No hypoglycaemia as monotherapy
  • Weight neutral (may aid weight loss)
  • Good glucose lowering effect
275
Q

side effects of SGLT2i?

A
  • Urinary infections + candidiasis
  • Hypovolaemia (uncommon)
276
Q

rare SE of SGLT2i?

A
  • DKA (rare)
  • Fournier’s gangrene (rare)
277
Q

GLP-1 analogue?

A
  • No hypoglycaemia as monotherapy
  • Weight loss
  • Good glucose lowering effect
  • Injectable
278
Q

glp-1 analogue - side effect?

A
  • GI side effects – N & V
  • Risk of pancreatitis
279
Q

GLP-1 analogues should be avoided in?

A

medullay thyroid Cx

280
Q

DKA treatment summary?

A
  • fluid resus
  • treatment of ketosis and hyperglycaemia w insulin infusion
  • management of potassium effects
  • transition back to usual insulin regime
281
Q

differences of HHS comp too DKA?

A
  • IV fluids before insulin – essential
  • No IV insulin until glucose stops falling by 5 mmol/hr using IV fluids
  • If IV insulin needed then use low dose (0.5 units/kg/hr)
  • Need for thromboprophylaxis
  • Look for infection + treat
  • Foot care
282
Q

characteristic features of HHS

A
  • hypovolaemia
  • marked hyperglycaemia (>30mmol) without sig hyperketoneaemia (<3mmol) or acisdosis (ph >7.3)
  • high osmolarity >320
283
Q

hypo - adults who are unconscious and/or having seizures and/or are very aggressive w IV access?

A
  • If IV access available, give 75-100ml of 20% glucose over 15 minutes, (e.g. 300-400ml/hr).
  • If IV access available, give 150-200ml of 10% glucose (over 15 minutes, e.g. 600-800ml/hr).
284
Q

hypo - adults who are unconscious and/or having seizures and/or are very aggressive - no IV access?

A
  • If no IV access is available then give 1mg Glucagon IM.
285
Q

graves radioiodine scan results?

A
  • thyroid will have homogenous uptake
  • pyramidal lobe visualization supports diagnosis
286
Q

Toxic multinodular goitre radiodione scan?

A
  • herotegnous thyroid appearancr rep a mix of overactive tissues and normal tissue
  • high radio-iodine uptake
287
Q

subacute thyroiditis radioidoine scan?

A
  • thyrotoxicosis secondary to leakage of stored hormone from an inflamed gland
  • v low uptake of radioiodine
288
Q

toxic nodule radioiodine scan?

A
  • almost always benign
  • focal inc uptake w suppression of surrounding tissues
  • high uptake
289
Q

Treating hyperprolactinoma - dopamine agonists?

A
  • cabergoline: causes less nausea than bromocriptine, adminstered once or twice a week
  • bromocriptine - daily
290
Q

Hypercal summary?

A
  • Bisphosphonates
  • Calcitonin
  • Corticosteroids (high Vit D, sarcoidosis)
291
Q

Hypercalcaemia >3.5 mmol/L =

A

EMERGENCY

  • IV 0.9% sodium chloride
  • IV Zoledronic acid 4mg over 15 min (once fully rehydrated)
292
Q

how do bisphosphonates work?

A
  • inhibit osteoclastic bone resportion
  • poorly abs from gut - orally best taken once a week on an empty stomach to avoid binding Ca2+ in food
293
Q

hypocalcaemia?

A
  • PTH def, vitamin D def
  • usually treated w vitamin D compounds
294
Q

hypocalcaemia Tx?

A
  • alfacalcidol (1α-hydroxycholecalciferol), calcitriol (1,25-dihydroxyvitamin D3or 1,25-dihydroxycholecalciferol) – can be used in renal failure
  • colecalciferol (vitamin D3), ergocalciferol (vitamin D2) – need a functioning kidney
295
Q

hypomagnesima and hypocalcaemua?

A
  • Severe hypomagnesemia can result in hypocalcemia as magnesium is a co-factor necessary for PTH production in the parathyroid glands.
  • correct Mg first
296
Q

comps of Severe hyponatreamia?

A
  • risk of osmotic demylination syndrome
  • too rapid rise or fall in serum Na
  • limit to no greater than 10mmol change in first day
297
Q

SIADH mX?

A
  • tolvaptan
  • decreases binding ot vasopressin at the V2 receptor, decreasing fluid secretion
298
Q

acute hyponatreamia management?

A
  • hypertonic saline - 3% NaCl
299
Q

Acute severe hyperkalaemia Mx?

A
  • defined as K+ >6.5
  • urgent IV treatment with calcium chloride or calcium gluconate
300
Q

what else can be used for acute hyperkalaemia?

A
  • IV injection of insulin with 50mL glucose 50%
  • salbutamol
301
Q

correcting acidosis w hyperkalaemia?

A

sodium bicarb (do not give in the same line as calcium salts - risk of precipitation)

302
Q

hyponatraemia symptoms?

A
  • Seizures
  • Obtundation
  • Respiratory failure
  • Nausea & vomiting,
  • Headache
  • altered mental status
  • Asymptomatic especially in chronic hyponatraemia (>48hrs onset)
303
Q

management

Hyponatreamia - SIADH?

A
  • fluid restruction to 1/L/ day and use of 3% sodium chloride infusion
  • or loop diuretic
304
Q

hypernatremia symptoms?

A
  • Lethargy
  • Weakness
  • Irritability
  • Seizures
  • Increased thirst
  • Spasticity
  • Hyperreflexia
  • Hyperthermia
  • Delirium
  • Coma if hypernatremia is acute (< 48 hours) and/or severe
305
Q

management of hypernatreamia?

A

isotonic saline

306
Q

causes of hypokalaemia?

A
  • loop and thiazide diuretics
  • hyperaldosteronism
  • GI losss - diarrhoea, vomiting
  • hypomag
307
Q

symptoms of hypokalaemia?

A
  • Muscle pain
  • Cramps
  • Weakness
  • Fatigue
  • Constipation
  • Syncope
  • Palpitations
308
Q

K+ of < 2.5

A
  • In <2.5mmol/L - paralysis starting from lower extremities then upwards, respiratory failure, ileus, tetany
309
Q

Hypokalaemia ECG?

A
  • flattened T waves
  • ST depression
  • U waves
310
Q

Hypokal managament?

A
  • Mild - sando-K oral
  • moderate - IV
  • severe (life threatening) - iV K+
311
Q

severe hyperkal =

A

> 6.5

312
Q

drugs causing hyperkal?

A
  • amiloride
  • ACE
  • heparin
  • NSAIDs
  • ciclosporin
313
Q

symptoms of hyperkal?

A
  • Weakness
  • Fatigue
  • Flaccid paralysis
  • Depressed/absent reflexes
  • bradycardia
314
Q

ecg in hyperkal?

A
  • tall tented T waves
  • prolonged PR
  • wide QRS
  • asystole
315
Q

stabilising the myocardium when potassium is > 6.5?

A
  • IV calcium chloride
  • IV calcium gluconate
316
Q

Hyperkal: shifting K intracellularly?

A
  • glucose
  • salbutamol
317
Q

hyperkal - removing it from the body?

A
  • sodium zirconium
  • calcium resonium
318
Q

what can be used in resistant hyperkal?

A

haemodialysis

319
Q
A

Year 3 (45 decks)

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