high-yield conditions Flashcards

1
Q

DPP4i

A

sitagliptin, linagliptin
used in T2DM
inhibits dipeptidylpeptidase-4 which inactivates incretins (glucagon-like peptide-1 [GLP-1] and glucose-dependent insulinotropic peptide [GIP]) which are released by intestines all day in response to food and prmote insulin secretion and suppress release of glucagon.
GI upset, headache, nasopharyngitis or peripheral oedema. Hypoglycaemia (less than in SUs) esp with other meds.
a small risk of acute pancreatitis, affecting 0.1–1% people taking the drugs. This should be suspected in patients experiencing persistent abdominal pain and usually resolves on stopping the drug.
CI: ✗type 1 diabetes or ✗ketoacidosis ✗pregnancy or ✗breastfeeding
do not reduce risk of vascular complications

β-blockers may mask symptoms of hypoglycaemia.

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2
Q

metformin

A

t2DM
biguanide. reduces hepatic glucose output by reducing glycogenolysis and gluconeogenesis and, to a lesser extent, increases glucose uptake and utilisation by skeletal muscle. can cause modest weight loss
GI upset, including nausea, vomiting, taste disturbance, anorexia and diarrhoea.
Lactic acidosis mainly in ppl with an intercurrent illness that causes metformin accumulation (e.g. renal impairment), increased lactate production (e.g. sepsis, hypoxia) or reduced lactate metabolism (e.g. liver failure).
dosage reduction required if the estimated glomerular filtration rate (eGFR) is <45 mL/min per 1.73 m2 and the drug stopped if eGFR falls below 30 mL/min per 1.73 m2.
CI: ✗acute kidney injury or ✗severe tissue hypoxia, e.g. in sepsis, cardiac or respiratory failure, or myocardial infarction.
withheld during ▴acute alcohol intoxication
Metformin must be withheld before and for 48 hours after injection of ▴IV contrast media

swallow tablets whole with a glass of water with or after food to minimise GI side effects.

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3
Q

SU

A

gliclazide
t2DM
Sulphonylureas lower blood glucose by stimulating pancreatic insulin secretion
associated with weight gain.
Dose-related side effects such as GI upset (nausea, vomiting, diarrhoea, constipation) are usually mild and infrequent.
Hypoglycaemia
Rare hypersensitivity reactions include hepatic toxicity (e.g. cholestatic jaundice), drug hypersensitivity syndrome (rash, fever, internal organ involvement) and haematological abnormalities (e.g. agranulocytosis).

Sulphonylureas should be taken with meals

β-blockers may mask symptoms of hypoglycaemia

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4
Q

insulin

A

t1dm
t2dm where oral therapy inadequate
diff choices -
rapid acting (immediate onset, short duration) – e.g. NovoRapid® (insulin aspart); short acting (early onset - 2-3 hrs delay in peak efffect, short duration) – e.g. Actrapid® (soluble insulin); intermediate acting (intermediate onset and duration) – e.g. Humulin I® (isophane or NPH insulin); and long acting (flat profile with regular administration) – e.g. Lantus® (insulin glargine), Levemir® (insulin detemir). Biphasic insulin preparations contain a mixture of rapid- and intermediate-acting insulins, e.g. NovoMix® 30 (30% insulin aspart, 70% insulin aspart protamine). Where IV insulin is required (hyperkalaemia, diabetic emergencies, peri-operative glucose control), soluble insulin (Actrapid®) is used.

hypoglycaemia - coma and death
When administered by repeated SC injection at the same site, insulin can cause fat overgrowth (lipohypertrophy)

Insulin regimens need to provide ‘peaks’ of insulin to deal with the glucose absorbed at mealtimes, and lower ‘basal’ levels in between. Examples include ‘basal–bolus’ regimens, e.g. Lantus® (glargine; long acting) taken once daily and NovoRapid® (insulin aspart; rapid acting) with meals and snacks; and twice-daily regimens, e.g. NovoMix® 30 (biphasic insulin). SC insulin is best prescribed by brand name.

rapid-acting: give immediately before meals.
biphasic insulin - administer immediately before a meal

Try to avoid giving ‘correction’ doses of insulin to treat hyperglycaemia in inpatients. It is generally better to tolerate transient, mild hyperglycaemia and instead adjust the patient’s scheduled insulin doses to avoid recurrence the next day. Correction doses add instability and can make titration of scheduled insulin more difficult.

t1dm -
1st line: multiple daily SC injection basal-bolus insulin regimens as the first line choice.Twice-daily or once daily insulin detemir should be offered as the long-acting basal insulin therapy, unless the patient is already meeting their agreed treatment goals on another insulin regimen. A rapid-acting insulin analogue is recommended as the mealtime insulin replacement eg insulin aspart (Novorapid)

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5
Q

cross-sensitivity within the beta lactams class of abx -

A

For carbapenems - CI in history of immediate hypersensitivity reaction to beta-lactam antibacterials.
Use with caution in patients with sensitivity to beta-lactam antibacterials.

for cephalosporins - Cross-reactivity between penicillins and first and early second-generation cephalosporins has been reported to occur in up to 10%, and for third-generation cephalosporins in 2–3%, of penicillin-allergic patients. Patients with a history of immediate hypersensitivity to penicillin and other beta-lactams should not receive a cephalosporin. Cephalosporins should be used with caution in patients with sensitivity to penicillin and other beta-lactams.

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6
Q

broad spec abx (carbapenems and cephalosprins) and wararin interaction

A

Cephalosporins and carbapenems can enhance the anticoagulant effect of warfarin by killing normal gut flora that synthesise vitamin K.

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7
Q

symptoms of angina and stable vs unstable

A

typically constricting chest pain with or without radiation to jaw or arms. Angina is “stable” when symptoms are always relieved by rest or glyceryl trinitrate (GTN). It is “unstable” when the symptoms come on randomly whilst at rest, and this is considered as an Acute Coronary Syndrome.

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8
Q

diagnostic ix for stable angina? and other ix pts shd have when presenting with angina

A

CT coronary angiogram

Physical Examination (heart sounds, signs of heart failure, BMI)
ECG
FBC (check for anaemia)
U&Es (prior to ACEi and other meds)
LFTs (prior to statins)
Lipid profile
Thyroid function tests (check for hypo / hyper thyroid)
HbA1C and fasting glucose (for diabetes)
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9
Q

Mx of stable angina

A

4 principles - RAMP
Refer to cardiology (urgently if unstable)
Advice regarding diagnosis, management and when to call an ambulance
Medical management
Procedural management

medical management:
immediate symptom control - sublingual GTN spray - as required during angina episodes. use once and wait 5 mins. if pain still there use again and wait 5 mins. if pain still there then call ambulance.
long term symptom control - either beta blocker or CCB (eg amlodipine)
Other options (not first line):

Long acting nitrates (e.g. isosorbide mononitrate)
Ivabradine
Nicorandil
Ranolazine

2ndary prevention of CVD - aspirin 75mg, atorvastatin 80mg. ACEi, beta blocker (already on for LT symptom relief)

procedural interventions:

  1. PPCI - primary percutaneous intervention with coronary angioplasty IF proximal or extensive disease
  2. CABG - in pts with severe stenosis not suitable for PPCI.

look out for midline sternotomy scar, great saphenous vein harvesting scar and brachial artery and femoral artery access scars.

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10
Q

ACS pathophys

A

ACS is usually the result of a thrombus from atheroscelrotic plaque which ends up partially or completely blocking a coronary artery. it is aminly made of platelets hence antiplatets

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11
Q

RCA supplies

A

right atrium
right ventricle
posterior interventricular area
inferior aspect of left ventricle

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12
Q

circumflex supplies

A

left atrium

posterior aspect of left ventricle

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13
Q

LAD supplies

A

anterioir aspect of left ventricle

anterior interventricular septum/area

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14
Q

how to diagnose ACS?

A

ACS symptoms do ECG

  1. ST elevation or new LBBB - STEMI
  2. ST depression or T wave inversion or no ECG changes BUT raised troponins - NSTEMI
  3. troponin lvls normal - unstable angina or other diagnosis
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15
Q

symptoms of ACS`

A

symptoms shd typically last longer than 20 mins and NOT be relieved by rest -
central constricting chest pain along with possibly -
nausea and vomiting
sweating and being clammy
feeling of impending doom
SOB
palpitations
pain radiating/in neck,jaw/shoulders/arms

Diabetic patients may not experience typical chest pain during an acute coronary syndrome. This is often referred to as a “silent MI”.

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16
Q

areas affected by infarction and corresponding ECG leads and artery

A

i,aVL,v5 and v6 - lateral MI - circumflex
v1-v4 - anterior MI - LAD
i, avl, v1-v6 - anterolateral MI - left coronary artery
ii,iii,avf - inferior MI - right coronary artery

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17
Q

troponins and diagnosing MI

A
Diagnosis of MI typically requires serial troponins (e.g. at baseline and 6 or 12 hours after onset of symptoms). howevere they are not specific and there are other causes - 
PE
myocarditis
aortic dissection
sepsis
chronic renal failure
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18
Q

Ix for someone presenting with possible ACS

A

obviously do abcde and ix alongside -

Physical Examination (heart sounds, signs of heart failure, BMI)
ECG
FBC (check for anaemia)
U&Es (prior to ACEi and other meds)
LFTs (prior to statins)
Lipid profile
Thyroid function tests (check for hypo / hyper thyroid)
HbA1C and fasting glucose (for diabetes)

PLUS -

Chest xray to investigate for other causes of chest pain and pulmonary oedema
Echocardiogram after the event to assess the functional damage
CT coronary angiogram to assess for coronary artery disease
19
Q

Acute ACS management -

A
  1. 300mg aspirin
  2. sublingual GTN spray
  3. oxygen if sats <94%
  4. morphine if required (IV)
20
Q

definitive mx of STEMI

A
Patients with STEMI presenting within 12 hours of onset should be discussed urgently with local cardiac centre for reperfusion therapy with either:
    Primary PCI (if available within 2 hours of presentation) (if eligible then prasugrel with aspirin unless taking oral anticoagulant then give clopidogrel with aspirin)
    Thrombolysis (if PCI not available within 2 hours) (egstreptokinase, alteplase and tenecteplase.) (here give ticagrelor with aspirin unless high risk of bleeding then consider +/-clopidogrel)

after either of these assess LVF, cardiac rehab and 2ndary prevention

IF above not possible then medical management with -
ticagrelor and aspirin if not high risk of bleeding otherwise clopidogrel and aspirin or just aspirin. then offer cardiology assessment and assessment of LVF and cardiac rehab and 2ndary prevention

21
Q

mx of NSTEMI/unstable angina post acute mx

A
fondaparinux unless high bleeding risk. perform GRACE (Global Registry of Acute Coronary Events) risk scoring (6-month risk of death or repeat CV event ). 
low risk (<3%) - consider conservative mx with ticagrelor and aspiring unless high bleeding then clopi and aspirin or aspirin alone. followed by assessment for LVF and cardiac rehab and 2ndary prevention.
intermediate or high risk (>3%) - if unstable then immediate coronary angiography with follow on PPCI if indicated. otherwise perform coronary angiography with follow on PPCI if indicated within 72hrs. offer prasugrel or ticagrelor with aspirin if no oral anticoag otherwise clopi with aspirin. only offer prasugrel once PCI intended. then assess LVF, cardiac rehab and 2ndary prevention
22
Q

complications of MI

A
heart failure DREAD
dressler's syndrome 
rupture of heart septum or papillary muscles (latter can result in severe mitral valve regurg and cardiogenic shock and pulm oedema)
edema ie HF
arrhythmias and aneurysms
death
23
Q

dresslers syndrome?

A

post-myocardial infarction syndrome
2-3 weeks after an MI.
caused by a localised immune response and causes pericarditis
It presents with pleuritic chest pain, low grade fever and a pericardial rub on auscultation.
It can cause a pericardial effusion and rarely a pericardial tamponade

Ix - pericarditis ECG - global ST elevation and T wave inversion
echocardiogram (pericardial effusion) and raised inflammatory markers (CRP and ESR)
mx - NSAIDs (aspirin / ibuprofen) and in more severe cases steroids (prednisolone). They may need pericardiocentesis to remove fluid from around the heart.

24
Q

2ndary prevention after ACS

A

6As and lifestlye modifications
Aspirin 75mg once daily
Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months
Atorvastatin 80mg once daily
ACE inhibitors (e.g. ramipril titrated as tolerated to 10mg once daily)
Atenolol (or other beta blocker titrated as high as tolerated)
Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)
**Dual antiplatelet duration will vary following PCI procedures depending on the type of stent that was inserted. This is due to a higher risk of thrombus formation in different stents.

lifestyle -
Stop smoking
Reduce alcohol consumption
dietary changes such as increased fruit and veg, less red meat, 2 oily fish a week, etc. encourage exercise
Cardiac rehabilitation (a specific exercise regime for patients post MI)
Optimise treatment of other medical conditions (e.g. diabetes and hypertension)

25
Q

types of MI

A

Type 1: Traditional MI due to an acute coronary event
Type 2: Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)
Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event
Type 4: MI associated with PCI / coronary stunting / CABG

26
Q

COPD and presentation and ddx to consider

A

non-reversible progressive obstructive airways disease almost always caused due to smoking.

presentation - long term smoker presenting with chronic shortness of breath, cough, sputum production, wheeze and recurrent respiratory infections, particularly in winter.

ddx - LUNG CANCER, fibrosis or heart failure. COPD does NOT cause clubbing. It is unusual for it to cause haemoptysis or chest pain. all these need investigating for a different cause.

27
Q

MRC (Medical Research Council) Dyspnoea Scale

A

used for assessing the impact of their breathlessness
grades:
1 - breathless on strenuous exercise
2 - breathless on walking up hill
3 - breathlessness that slows walking on flat surface
4 - breathlessness on walking on flat which requires person to stop and catch breath after 100m
5 - unable to leave the house due to breathlessness

28
Q

diagnosis of COPD

A

clinical presentation + spirometry
spirometry - obstructive picture. The overall lung capacity is measured by forced vital capacity (FVC) and their ability to quickly blow air out is measured by the forced expiratory volume in 1 second (FEV1).
Being able to blow air out is limited by the damage to their airways causing airway obstruction. Therefore in COPD:

FEV1/FVC ratio <0.7 The obstructive picture does not show a dramatic response to reversibility testing with beta-2 agonists such as salbutamol during spirometry testing. If there is a large response to reversibility testing them consider asthma as an alternative diagnosis.
29
Q

severity of COPD staging

A

The severity of the airflow obstruction can be graded using the FEV1:

Stage 1: FEV1 >80% of predicted
Stage 2: FEV1 50-79% of predicted
Stage 3: FEV1 30-49% of predicted
Stage 4: FEV1 <30% of predicted
30
Q

ix to carry out in someone presenting with chronic SOB

A

spirometry
Chest xray to exclude other pathology such as lung cancer.
Full blood count for polycythaemia or anaemia. Polycythaemia (raised haemoglobin) is a response to chronic hypoxia.
Body mass index (BMI) as a baseline to later assess weight loss (e.g. cancer or severe COPD) or weight gain (e.g. steroids).
Sputum culture to assess for chronic infections such as pseudomonas.
ECG and echocardiogram to assess heart function.
CT thorax for alternative diagnoses such as fibrosis, cancer or bronchiectasis.
Serum alpha-1 antitrypsin to look for alpha-1 antitrypsin deficiency. Deficiency leads to early onset and more severe disease.
Transfer factor for carbon monoxide (TLCO) is decreased in COPD. It can give an indication about the severity of the disease and may be increased in other conditions such as asthma.

31
Q

long term management of COPD`

A

support to stop smoking
annual flu vaccine and pneumococcal vaccine

  1. SABA or SAMA
  2. without asthmatic or steroid responsive features - LAMA + LABA (UMECLIDINIUM AND VILANTEROL)
  3. with asthmatic or steroid responsive features then LABA + ICS (BECLOMETASONE WITH FORMOTEROL)
  4. if 2 and 3 insufficient - LABA + LAMA + ICS (FLUTICASONE WITH UMECLIDINIUM AND VILANTEROL)
  5. Nebulisers (salbutamol and/or ipratropium)
    Oral theophylline
    Oral mucolytic therapy to break down sputum (e.g. carbocisteine)
    Long term prophylactic antibiotics (e.g. azithromycin)
    Long term oxygen therapy at home (used for severe COPD that is causing problems such as chronic hypoxia, polycythaemia, cyanosis or heart failure secondary to pulmonary hypertension (cor pulmonale). It can’t be used if they smoke)
32
Q

management of acute exac of COPD

A

Ix -
ABG - resp failure? acidosis? high bicarb? (chronic retainer)
Chest xray to look for pneumonia or other pathology
ECG to look for arrhythmia or evidence of heart strain (heart failure)
FBC to look for infection (raised white cells)
U&E to check electrolytes which can be affected by infection and medications
Sputum culture if significant infection is present
Blood cultures if septic
oxygen therapy -
use venturi mask and aim 88-92% unless in acute emergency then high flow 15L and can change it later.
if known to NOT retain then can aim 94-98%

if well enough to be managed at home -
Prednisolone 30mg once daily for 7-14 days
Regular inhalers or home nebulisers
Antibiotics if there is evidence of infection

In hospital:
Nebulised bronchodilators (e.g. salbutamol 5mg/4h 1st and if required add ipratropium 500mcg/6h)
Steroids (e.g. 200mg hydrocortisone or 30-40mg oral prednisolone)
Antibiotics if evidence of infection
Physiotherapy can help clear sputum

Options in severe cases not responding to first line treatment:
IV aminophylline
Non-invasive ventilation (NIV)
Intubation and ventilation with admission to intensive care
Doxapram can be used as a respiratory stimulant where NIV or intubation is not appropriate

33
Q

insulin and glucagon place of production

ketogenesis

A

insulin -produced by the beta cells in the Islets of Langerhans in the pancreas
glucagon - produced by the alpha cells in the Islets of Langerhans in the pancreas.

Ketogenesis occurs when there is insufficient glucose supply and glycogens stores are exhausted, such as in prolonged fasting. The liver takes fatty acids and converts them to ketones

34
Q

DKA main problems to sort out?

A
  1. ketosis and related acidosis
  2. dehydration - Hyperglycaemia overwhelms the kidneys and glucose starts being filtered into the urine. The glucose in the urine draws water out with it in a process called osmotic diuresis. This causes the patient to urinate a lot (polyuria). This results in severe dehydration.
  3. potassium imbalance - Insulin normally drives potassium into cells. Without insulin potassium is not added to and stored in cells. Serum potassium can be high or normal as the kidneys continue to balance blood potassium with the potassium excreted in the urine, however total body potassium is low because no potassium is stored in the cells. When treatment with insulin starts patients can develop severe hypokalaemia (low serum potassium) very quickly and this can lead to fatal arrhythmias.
35
Q

presentation of DKA

A
Polyuria
    Polydipsia
    Nausea and vomiting
    Acetone smell to their breath
    Dehydration and subsequent hypotension
    Altered Consciousness
abdo pain
    They may have symptoms of an underlying trigger (i.e. sepsis)

priority is fluid resuscitation to correct the dehydration, electrolyte disturbance and acidosis. This is followed by an insulin infusion to get the cells to start taking up and using glucose and stop producing ketones.

36
Q

diagnostic criteria for DKA

A

Check the local DKA diagnostic criteria for your hospital. To diagnose DKA you require:

Hyperglycaemia (i.e. blood glucose > 11 mmol/l) or sometimes known T1DM or T2DM on SGLT2i
Ketosis (i.e. blood ketones > 3 mmol/l) or ketones on urine dipstick
Acidosis (i.e. pH < 7.3)
37
Q

DKA mx

A

FIG-PICK

F – Fluids – IV fluid resuscitation with normal saline and continued IV fluids (e.g. 1 litre stat, then 4 litres with added potassium over the next 12 hours)
I – Insulin – Add an insulin infusion (e.g. Actrapid at 0.1 Unit/kg/hour)
G – Glucose – Closely monitor blood glucose and add a dextrose infusion if below a certain level (e.g. 14 mmol/l)
P – Potassium – Closely monitor serum potassium (e.g. 4 hourly) and correct as required
I – Infection – Treat underlying triggers such as infection
C – Chart fluid balance
K – Ketones – Monitor blood ketones (or bicarbonate if ketone monitoring is unavailable)

Establish the patient on their normal subcutaneous insulin regime prior to stopping the insulin and fluid infusion.

Remember as a general rule potassium should not be infused at a rate of more than 10 mmol per hour.

38
Q

long term mx of t1dm

A

MDT
pt education

Subcutaneous insulin regimes
Monitoring dietary carbohydrate intake
Monitoring blood sugar levels on waking, at each meal and before bed
Monitoring for and managing complications, both short and long term

insulin usually prescribed as a basal bolus regime with a long acting insulin once or twice a day and rapid-acting insulin analogue injected before meals.

Injecting into the same spot can cause a condition called “lipodystrophy”, where the subcutaneous fat hardens and patients do not absorb insulin properly from further injections into this spot. For this reason patients should cycle their injection sites.

39
Q

symptoms of hypoglycaemia

A

tremor
sweating
irritability
pallor

more severe hypoglycaemia - reduced consciousness, seizures, coma and death

40
Q

mx of hypoglycaemia

A

combination of rapid acting glucose such as glucose tablets/lucozade if pt is conscious and cooperative and slower acting carbohydrates such as biscuits and toast for when the rapid acting glucose is used up. Options for treating severe hypoglycaemia are IV dextrose and intramuscular glucagon.

41
Q

long term complications of t1dm

A

Chronic exposure to hyperglycaemia causes damage to the endothelial cells of blood vessels. diabetes causes suppression of the immune system and hyperglycaemia provides good environment for microorganisms

macrovascular - 
CAD
peripheral vascular disease causing poor healing, ulcers,etc.
increased risk of stroke
hypertension

microvascular -
retinopathy
peripheral neuropathy
nephropathy - especially glomerulosclerosis

infection related complications -
UTI
pneumonia
skin and soft tissue infections particularly in feet
fungal infections - oral and vaginal candidiasis in particular

other complications -
increased risk of DKA
hypoglycaemia
depression and anxiety

42
Q

diagnosing OA

A

diagnosis can be made without any investigations if the patient is over 45, has typical pain associated with activity and has no morning stiffness (or stiffness lasting under 30 minutes).

43
Q

Mx OA

A

patient education

Weight loss if overweight to reduce the load on the joint
Physiotherapy 
Occupational therapy 
Orthotics  (e.g., knee braces)

analgesia - stepwise -

Oral paracetamol and topical NSAIDs
Add oral NSAIDs (consider co-prescribing a proton pump inhibitor)
Consider opiates such as codeine

Topical capsaicin

Intra-articular steroid injections provide a temporary reduction in inflammation and improve symptoms.

Joint replacement can be used in severe cases. The hip and knee are the most commonly replaced joints.

44
Q

options for elective joint replacement surgery:

A

total joint replacement
hemiarthroplasty
partial joint resurfacing