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HDT 2.1 > SGT's > Flashcards

SGT's Flashcards

1
Q

what risks does amlodipine have for use in the elderly?

A

it is an antihypertensive; causes reduced baroreceptor function which leads to increased hypertension and increased risk of falls

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2
Q

what risks does aspirin have for use in the elderly?

A

it has risk of bleedings and for elderly it has higher risk of causing fatal or serious outcomes
older patients with cardiac disease and renal impairment can have higher risk when taking NSAIDs

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3
Q

what risks does metformin have for use in the elderly?

A

when they have eGFR of <30 ml/min/1.72m^2; risk of lactic acidosis

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4
Q

why do renal excreted drugs need dose adjustment in elderly?

A

older people have decreased renal excretion function

their eGFR will decrease

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5
Q

what is the difference between acute and chronic renal deterioration?

A

acute can be reversible with treatment whereas chronic can occur over time and isn’t reversible

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6
Q

what can allow you to see if renal deterioration is chronic or acute?

A
  • the creatinine levels; they’ll be outside of 40-120 micromol/litre and can tell eGFR from the level
  • urea levels; higher in blood than normal range so kidneys aren’t filtering it quickly enough
  • lithium conc
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7
Q

what drugs are renal excreted?

A
  • antibiotics
  • diuretics
  • beta blockers
  • digoxin
  • lithium
  • ranitidine
  • metformin
  • NSAIDs
  • calcium channel blockers
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8
Q

what are the normal ranges for sodium levels, potassium, urea, creatinine and lithium?

A 
K+ = 3.5-5.3
Urea = 2.5-6.5
Li= 0.4-1
Na+ = 133-149
Creatinine = 40-120 micromol/litre
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9
Q

what drug class is zopiclone and prochlorperazine?

A

zopiclone; sedatives and non-benzodiazepine hypnotics

prochlorperazine; antiphyscotics

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10
Q

what is prochlorperazine associated with, especially in the elderly?

A
  • acts on the brain
  • makes elderly patients NS more sensitive
  • sedative effect
  • associated with falls
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11
Q

how do sedatives affect falling?

A

sedatives slow reaction time and impair the balance causing elderly risk of falling to increase

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12
Q

risks of taking NSAIDs in elderly?

A

they exacerbate hypertension and promote renal function deterioriation

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13
Q

what would lithium concentration being high suggest?

A

that the kidney is damage and there is decreased renal function- AKI or CKI

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14
Q

what are important factors to consider for pregnant women?

A
  • immunisations; flu and hepatitis, MMR
  • make sure to get drug history and current medication
  • pre-natal vitamins are a good option for decreasing abnormal defects
  • need to look lifestyle choices
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15
Q

why is important to find out the drug indication before considering use in pregnancy?

A
  • do risks> benefits?

- fetal metabolism might affect dose conc. and so doses might need to be adjusted

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16
Q

when is the worst time to take drugs during pregnancy?

A

first term as it has highest risk of foetal defects so drugs can have serious side effects

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17
Q

should sumatriptan be given to pregnant women?

A

unless benefits > risks then no it should be avoided

not known to be harmful but should discuss with GP

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18
Q

what drugs shouldnt a pregnant women have whilst breastfeeding?

A

flucloxacillin and co-codamol as there are trace amounts in breast milk the might affect the baby

  • can affect babies stool due to flucloxacillin having Gi disturbance side effects
  • co-codamol can have opioid toxicity and cause breathing difficulties for baby
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19
Q

what can cause peripheral oedema?

A

calcium channel blockers

- vasodilation changes in pressure lead to fluid leaking into interstitial area

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20
Q

what interaction does grapefruit and CCB have? so can how grapefruit cause oedema

A

grapefruit interferes with CCB clearance and so increases its bioavailability
- inhibits CYP3A4 enzymes so body exposure to CCB’s increase - can also occur with statins
grapefruit causes increased CCB exposure causing more fluid to leak into interstitial area so more fluid build up so more oedema

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21
Q

what is the DDI of warfarin and amiodarone?

A

amiodarone reduces warfarin clearance by 44-55%
it also increases its anticoagulant effect and could lead to severe bradycardia with high doses
it inhibits CYP enzymes so blood will be thinner and so warfarin metabolism is inhibited

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22
Q

if patient has low TSH and high T3 as well as tremor, agitated, anxious and increase appetite what could this be? what drug can cause this?

A

hyperthyroidism

the use of amiodarone due to high iodine content

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23
Q

what do lisinopril and spironolactone together cause?

A

increased risk of hyperkaliemia
aldosterone receptor antagonist + ACE inhibitor
ACE inhibitor reduces levels of aldosterone which retains K+

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24
Q

why are steroid treatment cards issued to patients?

A

they are issued for patients with adrenal insufficiency and patients who have missed doses puts them at risk of adrenal crisis

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25
Q

what are long term side effects of oral CCS such as prednisolone patients should be aware about?

A
  • increase risk of severe chicken pox if never had before
  • makes patients more susceptible to infections and severe ones
  • if taken of CCS abruptly it can cause adrenal insufficiency and maybe death or hypotension
  • systemic CCS can leads to psychiatric moods e.g. euphoria or suicidal thoughts; should seek medical advice or be aware to withdrawal symptoms
  • increased weight gain and appetite; and diabetes so might need to start on insulin
  • can increase risk of gastric ulcer so PPL
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26
Q

effect of furosemide on the kidney?

A

inhibits reabsorption of salts from ascending loop of Henle in renal tubule such as Na+ and K+ and water by blocking their ion channels
cause CD to be less permeable and more urine to be passed out
it reaches by glomerular filtration and secretary mechanisms

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27
Q

what side effects can loop diuretics have?

A

if there is less salts and water being absorbed so there is electrolyte imbalance and might cause dizziness and headaches; low K+ and Na+ levels

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28
Q

what first line treatment should patients with type 1 diabetes and hypertension have?

A

either angiotensin converting enzyme inhibitors or angiotensin II receptor blockers if ACEIs not tolerated

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29
Q

what first line treatment should patients with type 2 diabetes and hypertension have?

A

thiazide diuretics, ARBs or ACE inhibitors

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30
Q

what class drug is bendroflumethazide? how does it effect the kidneys?

A

it is a thiazide diuretic
it causes excretion of water and sodium ions into the urine
treats fluid retention and produces more urine
blocks Na+ transport in the DCT and so more Na+ to CD - CD is less permeable

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31
Q

what’s the best line of treatment for stage 2 hypertension?

A

should be for over 55’s CCB and for under 55’s it should be ACE inhibitors

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32
Q

what are possible ADR’s and warning points for CCBs?

A
  • can cause dizziness due to electrolyte imbalance
  • nausea, fatigue
  • shouldnt crush or chew tablet only swallow it whole
  • for elderly lower doses should be used and adjusted depending on renal function
  • take in morning not night as it will cause you to urinate more ; so expect to urinate more
  • they should drink more fluid; look out for muscle spasms and hypokalaemia
  • can get stomach issues initially but they will go away
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33
Q

how should most neonates drugs be administered?

A

should be diluted with Glucose 5% and should be administered over a time range of 10-30 minutes and should be IV administered

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34
Q

what monitoring should you have with gentamicin and why?

A

blood samples should be taken before doses

  • renal and vestibular function should be monitored
  • can cause otooxicity
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35
Q

why is benzylpenicillin given less frequently to kids than adults and why does gentamicin have higher dose in adults than kids?

A

doses are lower in children as both are excreted renally and so accumulate in kidney so need more time for it to leave the children system

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36
Q

what is the best administration of doses to children?

A

should be tablets that are dispersed in water or given by injection by IV use - dilute

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37
Q

what are other treatments for coup?

A
  • CCS
  • dexamethasone
  • if its severe, use nebulised adrenaline
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38
Q

what is important to remember when treating adults for epilepsy?

A

should start at low doses and increase until seizures are controlled

  • consider the syndrome and if its not clear, type of seizure should determine treatment
    e. g. consider age or sex or co-morbidity of treatment
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39
Q

why would sodium valproate or phenytoin be the wrong treatment for epilepsy in kids?

A

if you increase the dose of these, the plasma conc can increase and cause toxic side effects

  • valproate shouldn’t be used In girls who can have potential childbirth
  • phenytoin can effect contraceptive pill dosing so wrong for women who are on pills or going through periods
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40
Q

what routes can be used for emergency treatment of epilepsy in kids?

A
  • rectal route of diazepam ; if oral route isn’t tolerated
  • in community EpiPen might be an option
  • buccal route of midazolam; cheek and gum in between as lining is thinner so quick absorption
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41
Q

what is desmopressin and how does it work?

A

it a vasopressin that causes vasoconstriction to increase the blood pressure
it also works on V2 receptors in collecting duct and inserts aquaporins to allow more reabsorption of water so urine is more concentrated

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42
Q

what’s the difference between vasopressin and desmopressin?

A

vasopressin is the endogenous ADH from the hypothalamus
desmopressin is the synthetic version of ADH and has a longer half life than vasopressin as it metabolised more slowly in the body; also more potent

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43
Q

how does desmopressin work?

A

desmopressin is the synthetic version of ADH
ADH will be released from the pituitary glands and travel in bloodstream to the V2 receptors that are on the basolateral membrane of the CD
the binding of ADH to the V2 raises cAMP levels and this causes intracellular vesicles to release ADQP2 and to let them fuse with the apical membrane
water is then reabsorbed from the CD by osmosis ; this gradient is bought by the high solute conc in medulla into mass recta

it replaces ADH which isn’t there stopping kidney from absorbing any water

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44
Q

if a patient stopped taking desmopressin after taking it for a while how would their serum osm and urine osm be affected?
how to calculate these two values?

A
  • serum osmolality would increase as less water and more salts
  • urine osmolality would decrease as more water in the urine and so dilute urine
    urine osmolality = urea x 1.25 mmol/L
    serum osmolality = (2 x serum sodium) + serum glucose + serum urea
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45
Q

why can drinking excessive water alongside desmopressin be harmful?

A 
drinking more than required 
more water in blood
dilutes Na+ in body = can lead to seizures 
can cause hyponatremia 
increase BV and BP
46
Q

what can rapid correction of serum sodium cause?

A

can lead to osmotic demyelination syndrome
leads to neurological events
should be monitored - Na+ levels every 6 hours for 2 days after starting treatment

47
Q

how do V2 receptor antagonists work?

A

thye bind to the V2 receptors on the basolateral membrane of the collecting duct
means less APQ2 channels are inserted into the CD so less aquaporins and so less reabsorption of water in CD so more water excreted in urine so dilute urine
this increase serum osmolality in body and stops cells from swelling

48
Q

why are some classes recommended for first line of treatment of hypertension for only some populations?

A

afro-carribeans have lower renin levels than other so dont respond well to ACE inhibitors- they should avoid ACE inhibitors to avoid dehydration

49
Q

if there is low PaCO2 and low HCO3- what does this mean?

A

pH has decreased as metabolic acidosis has occurred

50
Q

what are clinical consequences of metabolic acidosis?

A

proteins will dentaure, enzymes function lost, nerves are hypertensive and HR changes
can lead to diabetes and also organ failure so decreased cardiac output

51
Q

how to find how much solute (e.g. HCO3-) is needed to restore serum (that solute) to a specific value?

A

Vd x weight (kg) x (solute range you want - actual value)

should administer this amount of solute needed in small increments

52
Q

usual adverse effects of morphine?

A
  • nausea
  • vomiting
  • dizziness
  • confusion
  • respiratory depression; can lead to opioid toxicity
53
Q

how is morphine usually cleared from the body?

A
  • undergoes glucoronidation
54
Q

why can morphine cause opiate toxicity?

A

its active metabolites are more potent than normal morphine so accumulates in the body
- MG6 metabolite has an extended half life ; contributes to accumulation and so low clearance from the body

55
Q

how can you reverse opioid toxicity?

A

use an opioid receptor antagonist

  • attaches to receptors
    e. g. naloxone
  • has a life life of up to 2 hours and so reverse toxicity effect
56
Q

how should you consider dosing and drugs with patients that have renal function?

A

for drugs with active potent metabolites decreases their doses
to avoid accumulation of the metabolites so any toxicity
give drugs with shorter half lives
or drugs with fewer active metabolites and longer half lives such as methadone

57
Q

what is the relationship of eGFR and serum creatinine?

A

as serum creatinine doubles the eGFR halves

58
Q

what is the MoA for synthetic nucleoside analogues?

A
  • they work by interfering with the viral DNA chain and prevents it from growing
  • it inhibits and inactivates viral DNA polymerase
59
Q

why would phosphate levels be high in a patient?

A

as patients who have CKD mean phosphate isn’t being ecxcreted properly renally so it accumulates

60
Q

what are normal serum phosphate levels for Stage 4/5 for not on dialysis and for dialysis for CKD patients?

A

Stage 4/5 and not on dialysis - 0.8-1.4 mm/L

Stage 5 and on dialysis - 1.1-1.7 millimoles/L

61
Q

what does it mean if a gland in the neck is overactive?

A

the parathyroid gland is overactive so too much PTH is made; Ca+ levels rise high
- for patients with CKD they have decreased phosphate secretion and less Ca+ reabsorption

62
Q

what is calcium acetate and what does it do? how does it do this?

A

it is a phosphate binder and decreases the serum phosphate level - calcium acetate will bind to the phosphate and prevent it from being reabsorbed back into the bloodstream; so it must be excreted renally decreasing serum phosphate levels
- it has interactions with hormones and iron tablets

63
Q

how does alfacalcidol work?

A

it is a vitamin D supplement for VD deficiency

- it is hydroxylated so is activated and provides the supplements needed

64
Q

for any calcium and phosphate affecting medication what should a patient be aware of?

A

e. g. calcium acetate and alfacalcidol
- should monitor phosphate and calcium serum levels
- after any dose changes, calcium levels should be monitored twice a week until the patient is stable with the dose

65
Q

what is the role of cinacalcet? side effects?

A

it reduces release of PTH to decrease Ca conc. so reducing any overactive glands
- hypotension, vomiting, CV affects; arrhythmia or QT interval prolongation leading to ventricular arrhythmias

66
Q

what is the best way to diagnose a patient with hypertension?

A

they should have about three readings and should do take an ambulatory blood pressure reading over 24 hours with measurements every 30 minutes; then an average of these values taken
ABP
if not ABP use home blood monitoring with a measurement at night and one in the morning 2 readings each time for >4 days

67
Q

what are some non-pharmacological approaches to S1 hypertension?

A
  • diet
  • exercise
  • low Na+ intake
  • low alcohol intake
68
Q

what are first line treatment for hypertension with pregnant ladies or child-bearing potential?

A

you wouldn’t use ACE inhibitor as risk of teratogenicity
maybe CCB or beta blocker like nifedipine

  • make sure to recommend lifestyle choices and modification as well
69
Q

what is a BNP test?

A

a test that measures the level of a protein called BNP in your blood
normal level is <100pg/ml
higher it is, its more associated with heart failure and high BP

70
Q

with hypertension, for what age should beta blockers not be used as treatment?

A

for patients 60 and over and high doses of it shouldnt be used
CCB should be used alternatively

71
Q

should patients with risk of diabetes take beta-blockers?

A

no as beta blockers can increase blood glucose conc. and so increase diabetes risk
should take ACE inhibitors or ARBs as they are renal protectors so if diabetes cause nephropathy they can reduce this

72
Q

what’s the aim for patients who should have controlled hypertension?

A

around 150/90 mmHg

73
Q

when should you send a urinalysis for a microbiological culture?

A

only should be sent if she has had antibiotic treatment before or she has some sort of antibiotic resistance
if she is over 65 or if pregnant
or has kidney infection
for men it should be sent straight away if any suspicion

74
Q

what are first line antibiotic treatments for UTI?

A

if eGFR is less than 45 then nitrofurantoin but if not penicillin, fosfomycin
should do whole course of antibiotic to avoid resistance build up

75
Q

how does OTC potassium citrate work?

A

it makes the urine less acidic and dissolves any kidney stones
it removes discomfort but not recommended by NICE
no antibacterial effect
can take it to see if it helps but depends on other medications

76
Q

can NSAIDs be used in patients with hypertension and AKI?

A

ibuprofen is an NSAID and it blocks prostaglandins meaning that vasodilation cannot occur and so blood flow is reduced. the ibuprofen should be switched for paracetamol

77
Q

what are the risks of gentamicin?

A

it has risks of nephrotoxicity and ototoxicity
has a narrow therapeutic window
- it can accumulate in elderly
- it is excreted renally

78
Q

why do type II diabetes patients get CKD and how is it detected?

A

type II diabetes stops blood vessels in kidneys working and so reduced renal blood flow
proteins enter urine and cause haematuria
detected by seeing albumin in urine from tests

79
Q

what monitoring and counselling is needed before someone starts ramipril?

A
  • check renal function and electrolyte levels

- if increasing dose, these must be checked and must be within normal ranges

80
Q

how to find the ventricular rate from an ecg?

A

count the number of QRS complexes and then x6

81
Q

if the relationship between QRS complexes and P waves isn’t regular what is this?

A

it is an irregular heartbeat

it is called AV dissociation - no regular relationship- AV node or ventricles aren’t working properly

82
Q

how does calcium gluconate work on the heart?

A

it will cause hypercalcaemia which can lead to cardiac arrhythmias, vasodilation, bradycardia etc.
restores membrane potential of myocyte and stops them from being too excited
given slow IV infusion or directly or continuous infusion

83
Q

what kind of insulin lowers potassium levels?

A

short acting 50% insulin

give glucose to avoid hypoglycaemia and activates the Na K ATPase pump so influx of potassium can occur

84
Q

what risk does prednisolone have for immunocompromised patients?

A

they are immmunosuppressants and exerts glucocorticoid effects

85
Q

if you have a stone in you ureter how does that cause pain in the abdomen?

A

sensory fibres that supply the ureter enter spinal cord at T11-L2 and these fibres deliver the pain sensation to these parts of the body. it is called referred pain

it is shared innervation from the brain as well so referred pain
stone also causes inflammation

86
Q

how can a kidney stone cause pain?

A

it blocks the urinary flow

  • sensory innervation
  • pressure build up and so prostaglandins are released ; vasodilation is caused
  • hyper peristalsis of ureter can occur; cause inflammation, oedema, irritation and so the severe pain
87
Q

how can you help stones pass through ureters?

A

you could use alpha adrenoreceptor blockers- prevent epinephrine production and so vessel walls will relax and fluid transport can occur and so stone will pass out
alpha blockers prevent ureteral spasm and relaxes ureter smooth muscle
only give drugs is stone is less than 10 but if bigger than 10 offer surgery - for less than 5 they should wait

88
Q

what are side effects of giving drugs for stones?

A

alpha blockers can cause hypotension, dizziness and headaches
GI disturbances, nausea or dry mouth

89
Q

what are antipasmodics?

A

drugs that suppress muscle spasms
has an anti-muscarinic effect so inhibit spasms
are also anticholinergic

90
Q

what are side effects of antispasmodics like hyoscine butyl bromide?

A

can cause hypotension, tachycardia
can cause anaphylaxis
BNF says headache, constipation, drowsiness, palpitations and nausea
urinary tension is a side effect

91
Q

what are typical symptoms of urge incontinence, overactive bladder and stress incontinence?

A
  • urinating urgency

- when pressure exerted on bladder urine can lead; coughing laughing or sneezing

92
Q

what are the type of urinary incontinence you can have?

A
  1. stress; involuntary leakage on effort and no pelvic floor support and urethral sphincter is damaged
  2. urgency; involuntary league; cystitis
  3. mixed; involuntary leakage from both stress and urge
  4. overflow; chronic urine retention
93
Q

what could be some physiological or anatomical reasons for urinary incontinence?

A
  • levator ani muscles is pelvic floor support; this support becomes weak and non-existent
  • female urethra is shorter so any damage can cause this
  • can have detrusor muscle overactivity for urge urinary incontinence and pressure has increased; this can damage nerve supply of bladders
94
Q

what symptoms might make you lean towards urgent referral for urinary incontinence?

A
  • over 45
  • has potential bladder cancer
  • over 60 with heamaturia and dysuria or raised WBC
  • a recurrent UTI
95
Q

what are non-pharmacological things to do to help with urinary incontinence?

A

if high BMI then lose weight

  • pelvic floor muscle exercise
  • anticholinergics
  • have a bladder diary to keep track of anything unusual
96
Q

what medicine for first line treatment of overactive bladder?

A

anti-cholingerics
e.g tropium
1 tablet a day not in night and swallow whole

97
Q

what tests can you look at to see if anaemia is due to chronic renal disease?

A

look at eGFR ; should be <30 if due to CKD
look at cell counts and blood count; WBC, MCV and reticulocyte count
measure EPO levels
cells would be normal size in CKD
but low EPO levels if due to CKD
high urea makes RBC life shorter so high levels indicate anaemia due to CKD

98
Q

what is the mechanism of action of erythropoietin?

A

EPO is a glycoprotein; acts on erythroid progenitor cells in BM
- has a negative feedback system to control EPO production and so therefore RBC production
the EPO binds to EPO-R on RBC and activates signal pathway; proliferation and differentiation of precursor cells and producing erythrocytes

99
Q

side effects and cautions of EPO therapy?

A
  1. increased blood thickness so; DVT, embolism, epilepy

2. blood pressure; hypertension and blood clots

100
Q

what are risks of a blood transfusion?

A

it is temporary and can get infections due to antibodies and viruses, especially if blood isn’t a good specific match

101
Q

what is haemolytic anaemia?

A

when the antibodies of a persons immune system can cause damage to some of their red blood cells
can have 1. warm antibody type and 2. cold antibody type

102
Q

how does increased reticulocyte indicate heamolytic anaemia?

A

it shows that there has been RBC destruction as when this occur bone marrow sends signals to increase reticulocyte synthesis ; immature RBC

103
Q

what does high MCV, bilirubin and lactate dehydrogenase indicated?

A

MCV is increased due to RBC destruction causing Hb to be present outside of RBC
when RBC go through haemolysis LDH is released into plasma so high level
when Hb is broken down bilirubin is produced and so becomes elevated and released when RBC undergo haemolysis

104
Q

where does RBC destruction take place?

A

can have intravascularly with Hb into blood plasma

can have extravascularly and in spleen and liver and by macrophages

105
Q

how can an antibiotic cause haemolytic anaemia?

A

the IgG and IgM antibodies will bind to RBC surface antigens and cause RBC destruction and this is autoimmune or drug induced

106
Q

what can cause bruising?

A

a patient with anaemia

has low Hb count and low platelet count which means no causing a clot

107
Q

when taking immunosuppressants what should be monitored?

A
  • full blood count should be monitored every 3 months in patients taking azathioprine therapy
108
Q

how do B12 and folate contribute to erythrocyte production?

A

they are needed for proliferation during differentiation

having these deficiencies causes erythroblast synthesis and so anaemia

109
Q

how is B12 absorbed and how does it cause anaemia if deficient?

A

it binds to the intrinsic factor and taken into the gut
when you have a lack of B12 you get macrocytic anaemia
it is needed for RBC production

110
Q

side effects of iron tablets?

A

nausea
constipation
diarrhoea
GI discomfort

  • take on empty stomach but after food

HDT 2.1 (11 decks)

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