finals revision (mix of everything) Flashcards
BP targets for
1) patients with CVD, CKD, DM, OR framingham risk score > 20%
2) no risk factors or risk score < = 20%
3) Frail, old age eg. > 80yo
1) < 130/80
2) < 140/90
3) < 150/90 (less strict)
What is framingham risk score
Estimate 10 year risk of coronary death, non-fatal MI in asymptomatic patients without medical conditions which cause high risk (CVD, DM)
When to start treating for hypertension?
1) > 160/100
2) Grade 1: 140-159, with high risk score (>20%)
3) Grade 1: 140-159, and lifestyle modification after 3 months not working
4) High normal: 130-139 and high risk score -> treat if lifestyle modification not working
No need
130-139 + not high risk score
When should patient follow up for hypertension treatment?
Follow up:
- every 6 months
- every 3 months if patients have comorbidities eg. CKD, DM, or patients switched medications
What is CFS? Score and the meaning
1 - 9 (1 - 3 are fit, 4 - 6 are frail, 7-8 are very frail)
CFS 1 (Very fit)
Very active, exercise regularly and among the fittest for their age
CFS 2 (Fit)
No active disease, exercise occasionally
CFS 3 (Managing well)
Medical problems well controlled, not regularly active
CFS 4: (Very mild frailty)
Symptoms limit activity but not dependent on others for daily help. Tired during the day
CFS 5 (Mild frailty)
Evident slowing, need help with IADL (instrumental) eg. finances, transportation
CFS 6 (Moderate frailty)
Need help with all outside activities, IADL and some of basic ADL (bathing, stairs)
CFS 7 (Severe frailty)
Completely dependent for personal care. Stable, not at risk of dying
CFS 8 (Very severe frailty)
Completely dependent, approaching end of life. Cannot recover from minor illness
CFS 9 (Terminally ill)
Life expectancy < 6 months, not living in severe frailty
How does absorption change in elderly (4 pts)
1) Decrease in gastric acid secretion due to PPI or mucosal atrophy
2) Gastric emptying time prolonged
Caused by Anticholinergics, Opioids
Need to space apart food > 30 mins for bisphosphonates
3) Concurrent medications
Inducer of CYP: Phenytoin
PGPi: Clarithromycin, Amiodarone
PGP is a efflux pump, other drugs eg. Digoxin can be absorbed and cause toxicity
4) Transdermal route
Eg. using Fentanyl patch, Nitroglycerin patch
Increase absorption: epidermis and dermis thinning, heat pack
Decrease absorption: reduced cutaneous blood supply
how does distribution change in elderly
1) Body composition: Fat ↑, total body water and muscle ↓
2) Decreased serum albumin, Increased a1-acid glycoprotein
May result in clinically significant interaction with drugs
Eg. Phenytoin
3) Distribution into brain increased
More leaky BBB
Make elderly more sensitive to anticholinergic SE
Pgp activity lower
Which benzodiazepine should be used in elderly and why?
Use Lorazepam
Use short acting BZD and short course eg. a few days
Very sedating, increase fall risk in elderly
Increases risk of cognitive impairment, depression
Normal physiology of urinary tract
Bladder filling
Sympathetic NS activated / Parasympathetic NS blocked
B3 adrenergic receptor → bladder relaxed
A1 adrenergic receptor → smooth muscle contract, tighten urethra
Bladder voiding phase
Sympathetic NS blocked / Parasympathetic NS activated
M3 receptor in bladder → bladder contraction
What is metabolic acidosis?
How does metabolic acidosis occur?
Treatment?
When there is low base (bicarbonate) and high acid in the blood
When the kidney fails, acid H+ excretion is decreased, pH decreased
Excretion of NH3 and PO4 decreased
- NH3 and PO4 helps to remove H+
Treatment
1) Use alkalinising salts eg. Sodium bicarbonate, citric acid
- Citric acid requires liver function to be converted to bicarbonate)
How to treat COPD? (from ACE guidelines)
0 - 1 exacerbations
1) CAT < 10 (infrequent, less severe symptoms) -> LAMA
2) CAT ≥ 10 (frequent, more severe symptoms) -> LAMA + LABA
≥ 2 exacerbations OR ≥ 1 leading to hospitalisations
-> LAMA + LABA
+ Blood eosinophils ≥ 300 cells/uL
-> LAMA + LABA + ICS
Non pharm for COPD (4 points)
1) Reduce exposure to irritants
2) Vaccination (pneumococcal vaccine, yearly influenza vaccine)
3) Physical exercise
- eg. walking 3-4x a week for 20 - 30 mins
- Should still exercise even though breathless
4) Have a balanced diet
- Malnutrition can lead to poorer outcomes eg. impaired lung function, poor exercise tolerance, reduced QOL
Goals of therapy CKD associated anaemia
When to treat for CKD associated anaemia
Goal
- Hgb: 10-12, not above 13
- TSAT%: 20-30%
- Serum ferritin: 200 - 500 for HD patients, 100-500 for non HD patients
Treat when below goal
What do
- TSAT %
- Serum ferritin
mean?
TSAT% = (Serum Fe / TIBC) x 100%
- TSAT = Transferrin Saturation, the % of Transferrin which is saturated with iron aka carrying the iron
- Transferrin is the protein that transports iron
- Indicator of iron immediately available for delivery to bone marrow
Serum ferritin
- indicator of iron stores in the body
- acute phase reactant
(according to Chatgpt)
Explain TSAT %.
Why does transferrin aka TIBC have an inverse relationship with TSAT?
TSAT % = serum Fe / (TIBC aka Transferrin) x 100%
TSAT is measuring the saturation of transferrin protein, basically whether transferrin is saturated with iron
When iron is low:
- the body produces more Transferrin to capture and bind to the iron for transport. Hence there is high Transferrin, but meaning there will be many unsaturated Transferrin (Transferrin without Fe) -> low TSAT
When iron is high
- the body decreases Transferrin production as there is already alot of iron present. All the Transferrin present are highly saturated (carrying alot of iron) -> hence TSAT is high while Transferrin is low
What does absolute vs functional iron deficiency mean?
Absolute Fe deficiency = low TSAT, low Ferritin
Functional Fe deficiency = low TSAT, high Ferritin
- Functional: the function of TSAT is not working, hence even if i have high iron stores, it cannot be transported
What to monitor while on ESA? (3 points)
1) Adverse reactions eg. hypertension, seizures, vascular access thrombosis, flu-like symptoms
2) Pure red cell aplasia (antibodies against ESAs) due to SC Epoetin alfa (Eprex) or suboptimal storage conditions
3) Resistance to ESA
- if need significantly high doses of ESA to maintain Hgb
- common cause: iron, b12, folate deficiency (building blocks of erythropoiesis)
When should IV iron be withheld?
Adverse effects of IV iron
When patient undergoes infection
Can also switch to oral iron
Adverse effects
- Allergic reaction, hypotension, dizziness, dyspnea (can be minimised by decreasing dose or rate of infusion)
- iron overload (use Desferrioxamine iron chelating agent)
- Risk of infections
When should IV iron be monitored after starting
1 month, dont check immediately, wait for iron levels to fall
How to treat Asthma
Mild asthma, step 1 and 2 (symptoms < 4 days a week)
- Preferred: ICS-Formoterol PRN
Moderate asthma, step 3 (symptoms most days, waking up ≥ 1x a week)
- Preferred: Low dose ICS-Formoterol MART
Moderate asthma, step 4 (daily symptoms, waking with asthma ≥ 1x a week, low lung function eg. FEV1 < 60%)
- Preferred: Med dose ICS Formoterol MART, reliever: still low dose
Severe asthma, step 5
- Add on LAMA (Tiotropium)
- Consider biologics anti IgE, anti IL5, anti IL4, anti TSLP
- Trial 3 months high dose ICS LABA
- Oral corticosteroids eg. Prednisolone ≤ 7.5mg OD
non pharm for seizures (2 points)
ketogenic diet (low fat, high protein / fat diet, more vegetables)
Keep a seizure diary
which ASM are inducers (2 points)
Carbamazepine
Phenytoin
Adverse effects of ASM (3 points)
SJS / TEN
Suicide ideation (for Sodium valproate, Levetiracetam)
Hepatotoxicity
Thrombocytopenia (for Sodium valproate, Carbamazepine, Phenytoin)
What is status epilepticus?
Medications for status epilepticus
When seizure does not stop after 5 mins
First line: IV Lorazepam, Diazepam
Second line (if seizure does not stop after 20 mins): IV Valproic acid, Levetiracetam
