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Complex Pt 2 > Med Op > Flashcards

Med Op Flashcards

1
Q

5 metabolic syndromes

A 
High BP
insulin r
Low HDL cholesterol 
High triglycerides 
Visceral obesity
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2
Q

Role of pharm in obesity

A
  1. Cv risk assessments
  2. Lifestyle advice
  3. Behaviour modification
  4. Long term condition Mgt
  5. Interpreting evidence
  6. Individualising therapy and targets
  7. Pt involvement support and motivation
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3
Q

Number of obesity population in the world

A

2 billion

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4
Q

Waist circumference for obesity

A

> 35 inches women

>40 men

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5
Q

Trt options for obesity

A

Diet
Exercise
Medication
Surgery

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6
Q

Current drugs for obesity

A 
Orlistat
Lorcaserin 
Phentermine and topiramate
Bupropion / naltrexone 
Liraglutide
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7
Q

how many people in the uk are affected by HF? (uk has 66m people)

A

1m

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8
Q

the mortality rate of HF

A

40% death w/I first year of diagnosis

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9
Q

what are the 3 types of HF classification tools?

A

NYHA classification - most widely used
classed based on duration
or based on left ventricular ejection fraction

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10
Q

what are the 4 classes of NYHA of HF?

A 
class 1 - no limitation w physical act., normal LV function 
class 2 - slight limitation, comfort at rest, regular physical activity causes symp: fatigue, palpitation, dyspnoea
class 3 - marked limitation of regular physical activity, comfort at rest
class 4 - unable to carry out regular physical activity w/o discomfort, symptom at rest
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11
Q

describe the classification of HF based on LVEF

A

if LVEF > 40% heart failure with PRESERVED ejection fraction
< 40% HF with REDUCED ejection fraction
- not sued in practice due to the variability in heart imaging to assess function

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12
Q

what are the 3 types of HF

A
  1. left sided
  2. right sided
  3. congestive
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13
Q

describe the 2 types of left-sided HF

A
  1. reduced EF = systolic failure, LV cannot pump with enough force, reduced blood being pumped into circulation
  2. preserved EF = diastolic failure, pump is ok but LV chamber muscle is stiffen, so cannot fill adequately prior to each pump, so less blood enter circulation.
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14
Q

describe the physiology of right-sided HF and symptom

A

RV failure follows LV failure. increased blood return from lung to R chambers reduces pumping power. blood backs up venous system.
sym: swelling leg, ankles, abs

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15
Q

is congestive HF an emergency? what are the symptoms?

A

yes- congestive HF requires timely attention. congestion in body tissues: swelling in legs, ankles, lungs (SOB) –> pulmonary oedema –> resp failure

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16
Q

clinical features of HF

A
  1. symptoms of reduced o2 perfusion: SOB, fatigue, reduced exercise tolerance, tachycardia, tachypnoea, dyspnoea
  2. fluid overload: ankle swelling, SOB, orthopnoea, coughing, weight gain
  3. third heart sound: normal in young, disappear in old age. caused by a sudden deceleration of blood flow into the left ventricle from the left atrium.
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17
Q

HF is not a disease itself, it is a secondary consequence. causes of HF
CHDVE

A
  1. 80% of HF cases is due to coronary artery disease (CAD) eg MI, ischaemic myocardium reduces contractility.
  2. cardiac hypertrophy - thickening of heart muscle, reduce contractility.
  3. dilated cardiomyopahty - muscle dilate and ventricles get further apart caused by vitamin/thiamine deficiency. malnutrition, alcohol&drug abuse.
  4. valvular heart disease
  5. endocrine diseases eg adrenal dysfunction, Cushing due to ex glucocorticoid, diabetes, amyloid(plaques in heart), malignancy
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18
Q

more causes of HF

A 
1 thromboembolic complications (increase pulmonary pressure causing RH failure)
2 ischaemia
3 mechanical complications 
4 inflammation 
5 arrhythmias
6 hypertension
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19
Q

symptoms of worsening HF

A
  • increased SOB, reduced exercise tolerance
  • weight gain >2kg in two days
  • new orthopnoea (can’t breathe when lie down)
  • paroxysmal nocturnal dyspnoea
  • worsen of oedema or ascites
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20
Q

diagnostic tools of HF

A
  1. sign& symptoms
  2. eletrocardiogram
  3. echocardiogram
  4. chest x ray - check fluid overload and muscle thickening
  5. FBC - natriuretic peptides
21
Q

acute mgt for HF

A
  1. oxygen, target 92-96%
  2. morphine for SOB
  3. nitrates for pulmonary congestion
  4. diuretics for fluid retention (0.5-1kg loss per day)
  5. inotropes for hypopergusion (dopamine, dobutamine, A, NA)
22
Q

chronic mgt of HF

A

1st ACEI +BB
2nd spironolactone (Aldo antg)may used instead of ARB. hydralazine + isosorbide dinitrate (afro-caribbean or RF or not responding to ACEI)
3rd digoxin, ivabradine
others to trt HT, simvastatin, anti platelet/coagulants

23
Q

s/e of ACEI

A

angioedema
hyperkalaemia
renal dysfunction
dry cough - ARB

24
Q

most of ACEI are prodrugs that need to be metabolised in the liver except from…

A

lisinopril

captopril

25
Q

which three medical conditions are contra indicated for BB and why

A 
respiratory disease eg asthma --> SOB
diabetes --> cold peripheries, mask autonomic resp to hypo (shiver, faint etc)
heart block (bradycardia)
26
Q

the only 3 licensed BB for HF

A

carvedilol
metoprolol
bisoprolol

27
Q

MOA of neprilysin inhibitors

A
  • prevent the break down of natriuretic peptides by neprilysin (peptides reduces BP, BV, strain on heart)
  • paradoxically increase agII level, increase BP, thus given w ARB- valsartan
28
Q

example of neprilysin inhibitor

A

sacubitril prodrug –> sacubitrilat active drug

29
Q

use and cautions w neprilysin inhibitor eg sacubitril

A

used in mod to severe HF LVSD< 35%
liver impairment
NOT to be given w/I 36h of last dose of ACEI, give w next ARB dose

30
Q

MOA of digoxin

A

block Na/K ATPase, increase Na inside cell, K outside cell. accumulation of high conc of Na cause indirect activation of reverse of 3Na/Ca exchanger. increase Ca inside cell - SERCA pump - sarcoplasmic reticulum - contraction

31
Q

what to look out for when switching digoxin from IV to oral

A

increase dose by 20-33% to maintain same plasma conc

32
Q

when should you take digoxin level as it has narrow therapeutic window? what is the range

A

take level 6h after dosing, within 5-7 days of starting

1-1.5ng/ml

33
Q

what type of drug is ivabradine,
when is it used
how is it metabolised
direction of adm

A

SAN blocker (sinoatrial node) slows HR
used instead of/ additional to BB, used in NYHA class 2-4 w EF<35, RHR>75 target 60
metabolised by CYP3A4
take w food increase absorption by 20-30%

34
Q

what are the other medicine / trt may be needed for HF

A
  • iron tablet for anaemia, improve o2 perfusion to tissues NYHA2-3
  • coronary revascularisation
  • cardiac resynchronisation (pacemarker)
  • intracadiac defibrillators (prevent sudden death 50%) ICD
  • cardiac transplant (in cardiomyopathy- thicken/scar of heart tissue)
  • ventricular assist devices
35
Q

counselling advice for HF

NCSCAP

A
  • DIET reduce fluid, salt, potassium intake (less ready meal, avoid salt sub (often K), increase fruit veg, reduce saturated fat
  • exercise
  • smoking cessation
  • immunisation - vaccinations
  • no DRUGS: NSAIDs- COX2 inhibitor, sodium containing antacids,
  • corticosteroid (K flow, irregular HB),
  • antiarrhythemic agents (not BB). amiodarone
  • CCB (avoid diltiazem, verapamil = -ve inotropic)
    pioglitazone- worsen HF. metfrmin- RF
36
Q

wound healing process

A
  1. haemastatis: platelet begin the process of healing by releasing mediators eg GF
  2. inflammation: swelling, warmth and pain. bac and cell debris are removed from body by biochemical reactions (autolysis)
  3. proliferation: granulation/connective tissue forms on wound bed to repair the cell matrix
  4. maturation/remodelling: dermal tissue remodelled to form a scar
37
Q

What stops wounds from healing?

A
  1. inflammatory mediators: damage GF and ECM

2/ wound infection: bac release MMPs and enzymes that reduce GF and degrade fibrin (blood clot)/ECM

  1. biofilm: complex structure of microorganisms that adhere to wound surface, create physical barrier
  2. hypoxia- reduce fibroblast and collagen migration. production
  3. poor nutrition- lack of protein, reduce fibroblast formation. remain in infamy state
38
Q

Wound Bed Preparation

Barriers To Healing?

A
  1. dead tissues (necrosis) foster pathogenic bac., reduce migration of cells req for inflammation of wound healing (inflammatory mediators, GF, fibrin, fibroblast, collagen)
  2. bacterial colonisation- biofilms prevent healing and break down healthy cells in a wound. (60% present)
  3. too much ‘wrong’ exudate - chronic wound exudate contains proteolytic enzymes that destroys GF. ECM
  4. senescent cells - no longer responding to GF which promote healing. not dividing
39
Q

Wound assessment models - TIME

All four areas of the TIME acronym need to be addressed at each wound assessment.

A

T- tissue (non-viable) assess tissue type (necrosis/slough/granulation), debridement (removal of cellular debris to restore wound bed)

I- infection/inflammation. assess need for antiseptic/ systemic Abx. reduced inflammatory mediators and protease. increase GF

M- moisture imbalance - assess exudate, normally high in proteolytic activity damages wound bed and ECM.
- desiccation (slow epi migration) and ex fluid (maceration of wound margin)
use of NPWT/moisture balancing dressing to provide closed moist environment

E- edges - assess if wound contraction and epithelialisation is progressing. use EMT, laser therapy, US therapy, NPWT. reduction in wound area.

40
Q

what are the antimicrobial dressing used in clinic

A

silver, iodine, PHMB (Polyhexanide), honey dressing

41
Q

what are characteristics of chronic wound - prolonged inflammatory response

A 
increased MMP/ protease activity 
persistence of inflammatory cells
prolonged degradation of ECM
suppression of GF
biofilm present
42
Q

definition of debridement

A

The act of removing necrotic material, eschar, devitalised tissue, serocrusts, infected tissue, hyperkeratosis, slough, pus, hematomas, foreign bodies, debris, bone fragments or any other type of bioburden from a wound with the objective to promote wound healing

43
Q

target of debridement

A

remove bioburden, necrosis, slough, foreign bodies
decrease risk of infection, ex moisture, odour
stimulate cell migration, edge contraction, epithelialisation
improve QoL

44
Q

debridement methods

A

autolysis (use of moist dressing eg hydrogel, hydrocolloids to promote clear of dead tissue by body’s own enzymes)

Larvea / maggot therapy

mechanical (dry gauze)

hydro-surgical (high pressure saline)

US (disruption, fragmentation)

sharp by bedside (scalpel, specialist only)

surgical (invasive, anaesthesia)

45
Q

describe Larval Debridement therapy (LDT) or Biosurgery (classified as a medicine on FP10)

A
  • Lucila sericata (common green bottle fly) lie eggs
  • eggs disinfected
  • eggs hatch Fly hotel, form larvae
  • larvae are ascetically placed into pots (biobags)
  • larvae secretion is anti-bacterial, proteolytic enzymes cause slough degradation
  • feed on dead tissues by liquidaise them
  • produce ALKALINE pH by metabolite ammonia
46
Q

wound care decision parameters

A
  • pt envrionment
  • pt perference
  • skills of care giver
  • resources
  • age and co-morbidities
  • pain
  • QoL
  • guidlines
47
Q

Debridement process cycle

A
  • diagnosis (TIME)
  • decision (outcome and techniques)
  • add on (trt inf)
  • review
  • goal achieved?
  • repeat
48
Q

contraindications and cations of larvae DT

A
  • not to be used on wound that likely to BLEED/ near major BV
  • not used if pt on ANTICOAGLANTs where CF is NOT within range
  • maintain MOISTURE level, checked DAILY, wet with sterile saline
  • PSEUDOMONAS inf can reduce larval viability/efficacy
49
Q

prescribing of larvae DT

A

FP10, by GP. specialist, indendpent NOT supplementary rxer.
specialist nurse under directive PGD/ hospital -ok
ONCE only section on drug chart in hospital

Complex Pt 2 (4 decks)

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