Geri's / GP / General med stuff you forget Flashcards

1
Q

Lewy Body dementia presentation and treatment

A

Fluctuating cognitive impairment, visual hallucinations (not unpleasent), later on there can be Parkinsonism.

Tx similar to AD (Acetylcholinesterase inhibitors and memantine depending on stages). Antipsychotics should be avoided as precipitate parkinsonism (BDZs better)

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2
Q

How to differentiate PD from Dw/LB?

A

Lewy body dementia is more likely if dementia starts before or within 1 year of the onset of the parkinsonian symptoms. LBD also commonly causes visual hallucinations of people. Also a poor response to co-careldopa is a clue

Parkinson’s disease dementia is more likely if dementia occurs around 4-5 years after motor symptoms (but at the very least should be 1 year after).

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3
Q

What tool can be used to assess malnourishment/those at risk of becoming malnourished?

A

MUST

Measure BMI
note percentage Unplanned weight loss
establish acute disease affect and score.

2+ = immediate care with dietetic input.

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4
Q

What is the STOPP tool?

A

Screening tool of older person’s prescriptions

Identifies medications where the risk outweighs the therapeutic benefits in certain conditions

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5
Q

What is the START tool?

A

Screening Tool to Alert doctors to the Right Treatment. It looks at which medications should be used for certain conditions in patients 65 years or older.

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6
Q

What is frailty?

A

a clinical state of vulnerability, related to diminishing strength, natural ageing and a decline in physiological reserve. Resulting in an inherent risk of adverse clinical outcomes from minor stressors or challenges

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7
Q

What are the 4 syndromes in frailty?

(My Pa Cant Drive)

A

Malnutrition
Physical impairment
Cognitive impairment
Depression

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8
Q

What does the Fried Model suggest the frailty phenotype is?

A

3 or more of following:
* Unintentional weight loss
* Weakness (poor grip strength)
* Self-reported exhaustion
* Slow walking speed
* Low level of physical activity

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9
Q

What is Rockwood clinical frailty score?

A

9 point score that summarises general level of frailty.
You just score 1-9 based on clinical judgement

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10
Q

What is frailty index

A

A count of health deficits, the more deficits the more frail and greater risk of death.

Number of deficits an individual has / total number of deficits considered
Very fit <0.09, mild frailty 0.27, severely frail 0.42.

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11
Q

5 physiological marker’s of frailty

A
  • Increased inflammation – chronic inflammation due to dysregulation of multiple systems
  • Elevated insulin and glucose levels in fasting states
  • Low albumin
  • Raised D-dimer
  • Low vitamin D levels.
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12
Q

Some interventions for frailty

A

Vit D, diet, exercise (PT input), reduce polypharmacy, home adaptations, manage comorbidities

Prevent Cx

CGA is gold standard.

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13
Q

Name intrinsic and extrinsic RF for falls

A
  • Intrinsic – female, Cognitive decline, visual deficit, muscle weakness, causes of syncope
  • Extrinsic – polypharmacy, bifocal glasses, walking aids, footwear, home hazards
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14
Q

What is the triad of rhabdomyolysis symptoms and how is it treated?

A

myalgia, weakness, and myoglobinuria (tea-coloured urine).

IV fluids, dialysis if severe.

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15
Q

What are the 3 main categories of syncope (and 3 subtypes of reflex syncope)

A

Cardiac - arrhythmias, structural heart disease
Othostatic hypotension
Reflex syncope (NMRS)
- Vasovagal - mediated by emotiona stress or orthostatic stress
- Situational - post-prandial, cough/sneeze, postmicturition, playing wind instrument
- Carotid sinus syndrome

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16
Q

Describe pathophysiology of carotid sinus syndrome (CSS)/carotid sinus hypersensitivity and why it is more common in the elderly

A

Any pressure, e.g. neck turning, tight collars, shaving, leads to stimulation of the carotid sinus. The brain thinks we have hypertension causing a fall in HR and BP (vasodilation)
More common in elderly as the carotid baroreceptors get more sensitive as we age.

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17
Q

State 5 symptoms and 3 signs that indicate a cardiac cause of syncope

A

Syncope on exertion
If LOC occurs while supine (rules out postural)
Collateral cardiac Sx - palpitations/chest pain
PMHx of heart disease
FHx of sudden death

Signs - raised JVP, 3rd/4th heart sounds, pulmonary oedema.

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18
Q

Name 2 drugs that can help treat orthostatic hypotension

A

Fludrocortisone - aldosterone agonist
Midodrine - alpha agonist that increases BP

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19
Q

Define orthostatic hypotension and name 5 causes

A

Diagnosed as systolic BP drop of >20mmHg or diastolic BP drop of 10mmHg within 3 mins of standing. Also, if systolic drops <90 from any starting point.

Many conditions can cause it:
- Dehydration (fever, vomiting, diarrhoea, blood loss)
- Cardiac - bradycardia, AS, HF (heart cannot compensate for postural drop)
- Endocrine - Adrenal insufficiency (addison’s, less adrenal hormones = hypotension), DM (autonomic neuropathy)
- Neurological - PD, MSA, dementia (any autonomic neuropathy)
- Drugs - Tamsulosin/alpha blocker causes dilation of venous vessels lowering BP), diuretics, TCAs.

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20
Q

What is Barthel index?

A

A scale covering 10 basic ADLs used to establish degree of dependency. Usually out of 100, modified is /20.

Doesnt detect issues in mental functioning

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21
Q

What is Berg balance test?

A

Covers 14 everyday tasks, more basic than ADLs used in Barthel (e.g. transfer, sitting, standing etc.)
Does not assess gait

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22
Q

What is NEADL?

A

Nottingham extended ADL

Assess 22 instrumental ADLs (more complicated ADLs like “travel on public transport”).
Goes beyond the ceiling that can happen in BI.

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23
Q

What is Timed up and go test

A

It assess frailty/functioning

Sit, walk 3m, turn around and comeback and sit.
Tests transferring, static balance, dynamic balance, gait and cognition can all adversely impact upon the timed-up-and-go test.

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24
Q

What is normal AMT score?

A

8 or above (8, 9, 10)

It gives a quick overview of cognitive function - memory and orientation.

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25
Q

What is MOCA?

A

Montreal Cognitive Assessment

A screening tool for MCI. Useful in early AD.
Discriminates between normal cognition and MCI, but less good at getting severe CI.

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26
Q

Describe aetiology of pressure sores (acquired & inherited)

A

Acquired if they occur within a care facility
Inherited if pt moves into a facility with ulcer already present

Ulcers usually multifactorial
- Limited movement
- Sensory impairment
- Malnutrition/dehydration
- Obesity
- CI
- Urinary/faecal incontinence
- reduced tissue perfusion

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27
Q

What are the stages of pressure ulcers (1 to 4) and there Tx

A

Stage 1 - non-blanching erythema (intact skin). May feel warm and painful.
Stage 2 - partial thickness skin loss (epidermis/dermis) without slough. It is a superficial ulcer.
Stage 3 - full thickness skin loss, with loss of SC down to (but not through) underlying fascia. Slough or eschar may be present
Stage 4 - full thickness tissue loss w/ exposed bone/tendon/muscle.

Tx with prevention mainly (SSKIN - support surface (cushions), skin assessment, keep moving, incontinence/moisture, Nutrition and hydration)

Hydrocolloid dressings/hydrogels help healing. Avoid soaps.
Topical antimicrobial therapy (silver, honey, iodine) only when signs of local infection. Systemic abx if systemic sepsis or osteomyelitis.

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28
Q

What Ix for pressure ulcers?

A

Waterlow/Braden tools

Wound swabs not routine as most are colonised w/ bacteria. As such, decision to Tx based on clinical basis (e.g. surrounding cellulitis)

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29
Q

How is constipation in the elderly treated?

A

1st line lifestyle (oral fluid/fibre)

1st line medication = docusate (stimulant and softening properties)
May add macrogol (osmotic/softener)

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30
Q

Describe stimulant, osmotic, bulking laxatives indication/CI and SE

A

Stimulant - senna, danthron (palliative). Useful in older patient w/ normal stool but reduced motility. Increased motility can cause cramps.

Osmotic - lactulose, macrogols. Useful for hard stools/painful defacation. Require adequate oral intake and can cause dehydration.

Bulking - fybogel, methylcellulose. Good for inadequate fibre/small hard stools. Can cause abdo distension.

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31
Q

What are the 4 components to ageing

A
  • A universal process – occurs in all individuals of the same species
  • Intrinsic – endogenous factors predisposing to particular patterns of ageing
  • Progressive – occurring throughout life and present to a lesser degree in younger adults
  • Deleterious – changes to the individual associated with ageing must be “bad”.
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32
Q

What is primary and secondary ageing

A

Primary ageing is the interplay of intrinsic factors, such as the genetic makeup of an individual, and extrinsic factors, such as smoking, diet and exposure to UV light.
Secondary ageing is the adaptive response to primary ageing, which may not always be negative. An example would be writing things down due to a poor memory.

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33
Q

Physiology of ageing - what happens to:
A) Body fat and water distribution
B) Bone and muscle mass, and why
C) Immune system
D) CV system

A

A) Proportion fat increases, becomes central. Decrease total body water (cell shrinkage - ICF loss).
B) Reduced due to disuse atrophy, reduced testosterone/GH, impaired protein synthesis
C) Immunosenescence - B cell numbers are preserved but decreased antibody production (increased autoantibody). T cell numbers decrease.
D) Reduced elastin, increase collagen.

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34
Q

Describe 1, 2, 3 treatment of stress incontinence

A

1st line - physio/pelvic floor muscles. Cause increased urethral pressure. Also lifestyle - weight loss, stop smoking, reduce caffeiene.

2nd line - Duloxetine (SNRI) increases contraction of urethral sphincter by increasing adrenaline?

Surgery - sling, colposuspension etc.

35
Q

Describe urge incontinence 1, 2, 3 management

A

1st - bladder retraining
2nd - anticholinergics (oxybutynin), an M2/3 receptor antgonist that decreases detrusor excitability by inhibiting PSNS.
3rd line - Mirabegron - beta 3 agonist, relaxes detrusor.

May consider botulin toxin 6-9monthly injection.

36
Q

SHATTERED causes of osteoporosis

A

Steroids
Hyperthyroidism and hyperparathyroidism
Alcohol and tobacco
Thin (BMI<22 - reduced skeletal loading)
Testosterone decreased (increased turnover)
Early menopause (oestrogen protective)
Renal or liver failure (affect vit D metabolism)
Erosive bone disease (e.g. RA, myeloma)
Dietary calcium insufficiency/malabsorption

37
Q

What causes S4 and S3

A

S4 is atria contracting forcefully against stiff ventricles (associated with low compliance - HF, LVH, HTN)

S3 is diastolic filling, normal in <30. Heard in LV failure, constrictive pericarditis, MR.

38
Q

Most common cause of HF in developed world and africa

Causes of HF-REF and HF-PEF

A

IHD most common cause in developed world. HTN most common cause in africa.

HF-REF - LV systolic impairment (LVEF <40%). IHD, MI, HTN.
HF-PEF - Inability of LV to relax/fill (LVEF >50%). AS, chronic HTN, constrictive pericarditis.

39
Q

Which drugs do you want to avoid in HF?

A

NSAIDs - cause fluid retention by damaging glomerulus
Cardioselective CCBs - diltiazem / verapamil. Negative inotropes.

40
Q

Which drugs do we give to treat HF?

A

First line - ACEi/ARB (dilates blood vessels and reduces aldosterone) + non-cardioselective BB (carvedilol) prevents remodelling of heart and reduces mortality.

Symptoms - diuretics (furosemide) reduces preload. Can add spironolactone as no risk of hypokalaemia. Help breathlessness.

Digoxin and hydralazine/ivabradine also help.

41
Q

X-ray changes in HF

A

Alveolar oedema (bat wing shadowing)
kerley B lines (interstitial oedema)
Cardiomegaly
Dilated upper lobe vessels
Effusions (pleural)

42
Q

Mx of STEMI, initial and if </>12hrs, and post MI

A

MONA - morphine, oxygen, Nitrate/GTN, aspirin (and clopidogrel/ticagrelor)

PCI/CABG if within 12hrs of symptom onset and can be delivered within 2hrs
Fibrinolysis if within 12hrs symptoms but PCI not possible in <2hrs
If >12hrs symptom onset, medical Mx (MONA)

2nd prevention = Block An ACS (Beta blocker (propranolol/carvedilol), ACEi, Aspirin, Clopidogrel, Statin)

43
Q

Cx of MI (DREAAD)

A

Death
Rupture
Edema - due to HF following MI, give furosemide.
Arrhythmias (most common Cx within 24hrs)
Aneurysms
Dressler’s syndrome - 2o form of pericarditis.

44
Q

ECG changes seen with NSTEMI

A

ST depression and/or T wave inversion and pathological Q waves

45
Q

Mx of NSTEMI

A

Acute – MONAC
Calculate GRACE score – 6 month risk of another cardio event.
o Low risk (predicted 6month risk <3%) then conservative Mx (Ticagrelor + aspirin unless bleeding risk).
o High risk (predicted 6month risk >3%) then immediate angiography if unstable, or within 72hrs. Based on the findings we may do a PCI.

2nd prevention the same.

46
Q

Unstable angina Mx

A

MONA
2nd prevention

NB may be ST depression on ECG.

47
Q

Stable angina:
3 mechanisms
Most important RF (and 2nd)
Px
Gold std Ix
Mx (2nd prevention and Sx)

A

Stenosis of vessels - atherosclerosis (most common)
Increased distal resistance (e.g. LVH)
Anaemia

Hyperlipidaemia most important. Smoking 2nd - both for atherosclerosis

Chest pain/tightness radiating to jaw during exercise. Stops after 15mins or GTN spray.

CT coronary angiography

For Sx first line is beta blocker (reduce demand of heart) OR cardioselective CCB. If not then BB w/ non-cardioselective BB (nifedipine) as risk of asystole.
Prevention - aspirin, statins, ACEi. If persists PCI.

48
Q

How do arrhythmias present?

A

Palpations, dizziness/syncope, chest pain (myocardium not perfused properly), SOB, sudden death.

49
Q

Mx of SVT (acute and chronic)

A

Haemo unstable - emergency cardioversion
Haemo stable - Valsalva manoeuvre, carotid sinus massage, 6mg Adenosine. Cardioversion.

Beta blockers 1st line long term. Radiofrequency ablation 2nd.

50
Q

Causes of AF

A

Ischaemia (most common cause), idiopathic, CAD, HTN (hypertrophy of ventricles), HF, valve disease, thyroid disorders.

51
Q

Mx of AF

A

Haemo unstable - heparin + cardioversion (synchronised DC shock).

Haemo stable - DC conversion if rate >200.
- If onset >48hrs ago, rate control. Appropriate for older pts as more prone to ADRs of antiarrhythmics. 1st = cardioselective beta blocker (B1 slow HR at SAN), 2nd = cardioselective CCB (slow electrical activity)
- if onset <48hrs, rhythm control. Cardioversion (electrical/pharm) then beta blockers to suppress arrhythmias

Longterm do CHADS-VASc score to calculate need for anticoagulants

52
Q

AF vs flutter on ECG?

A

AF no p waves
Flutter - sawtooth flutter.

53
Q

Types of AV heart block and Mx

A

First degree - delayed AV conduction. PR interval >0.2s. No Mx, monitor for syncope, stop AV-nodal blockers (CCB, BBs)
Mobitz 1 (wenckebach) - PR interval prolongs until P wave fails to conduct = absent QRS, then repeats. As first degree
Mobitz 2 - QRS dropped every X p waves. Pacemaker
Third degree - P waves/QRS independent of each other. As above.

54
Q

SE of salbutamol

A

A beta 2 agonist. Can cause tachycardia and tremor from activating other receptors. Also hypokalaemia.

55
Q

What type of hypersensitivity reaction is asthma?

A

Type 1 - bronchial hyperresponsiveness to dust mite/faeces, cold air, exercise etc. Causes mast cells, eosinophils, T lymphocytes cause bronchoconstriction and increase secretions.

56
Q

Step 1-6 asthma management

A

1) SAB2A PRN (salbutamol/Terbutaline)
2) Add regular steroids (beclomethasone)
3) Add LTRA or LAB2A (salmterol)
4) increase ICS
5) Oral steroids
6) Hospital admission

57
Q

Signs of life-threatening asthma attack? 33 92 CHEST

O SHIT ME management for this

A

PEFR <33%
SpO2 < 92%
Cyanosis
Hypotension
Exhausation
Silent chest on auscultation
Tachycardia (not really)

Oxygen, salbutamol, Hydrocoritsone, Ipratropium (SAMA), Theophulline, MgSO4, escalate to anaesthatist for ventilation

Mild/moderate attacks - monitor, SABA and discharge with oral steroids

58
Q

Name a SABA, LABA, SAMA, LAMA

A

SABA - salbutamol and terbutaline
LABA - salmeterol
SAMA - Ipatropium bromide
LAMA - tiotropium

59
Q

Differentiate COPD and asthma

A

COPD is usually older smoker, constant (progressive) symptoms w/ no variation and variable response to steroids.
Inflammation is macrophages/neutrophils (CD8+ cells)

Asthma is younger, non-smoker with intermittent/variable symptoms with a good response to steroids.
Inflammation is with eosinophils (CD4+ cells)

60
Q

Causes of finger clubbing

A
  • Asbestosis
  • Bronchiectasis
  • Cancer (lung)
  • Do not say COPD/emphysema.
  • Empyema
61
Q

Describe emphysema and chronic bronchitis

A

Emphysema = pink puffers. There is dilation of lung tissue distal to terminal bronchioles. Leads to loss of surface area and air trapping (loss of recoil), decreases capacity for gas transfer. Smoke causes this by inactivating a1-antitrypsin (elastase inhibitor)

Chronic bronchitis = blue bloaters. Problem of airway (bronchiole) narrowing due to hypertrophy of muscles, hyperplasia of glands. Squamous metaplasia. Can lead to hypercapnia, hypoxic, cor pulmonale

62
Q

Px, Ix and Mx of COPD

A

Cough with sputum production, wheeze and breathlessness. Exacerbations have purulent sputum. Non-reversible (if liver signs A1AT).
Increased work of breathing - leaning forwards, accessory muscles, nasal flare, hyperinflated/barrell chest.

Ix - spirometry, CXR (hyperinflated), DLco (decreased, normal in asthma). Polycythamia.

First line - SABA.
Combination 2nd line:
- LABA + LAMA (tiotropium) if no asthmatic features
- LABA + ICS if asthma features
3rd line - triple therapy, LABA, LAMA + ICS.
4th - LTOT.

63
Q

bacteriology and abx for IE COPD

A

Haemophilus influenza most common. S.pneumonia, M.catarrhalis. (Virus like rhinovirus are 30%).

Doxy or co-amox if Hib.
Amox if S.pneu

64
Q

Define HAP and CAP and what is bacteriology?

A

CAP - outside of hospital. S.pneumonia (40%), chalmydia pneumoniae (13%), Mycoplasma pneumoniae (11%), Hib (5%), legionella pneumophilia (5%).

HAP at least 48hrs after hospital admission. S.aureus most common HAP. Also others.

65
Q

Pneumonia Px, Ix

A

Systemic Sx - sweats, rigors, pyrexia.
Chest - dyspnoea, productive cough (rusty sputum = S.pneuminiae)
Pleuritic chest pain (worse on deep breathing)
Signs - basal crackles, wheeze, pleural rub, dull to percuss.

Sputum MCS, cultures, FBC.

66
Q

Describe CURB65 and output (abx)

A

Predicts mortality
Confusion
Urea >7mmol/L
RR >30/min
BP <90 or <60
Age >65

0-1 outpatient. Amoxicillin 5 days (erythromycin)
2 admit. Amoxicillin + clarithromycin 5 days
3 or more often requires ITU. IV co-amox + clarithromycin.

67
Q

Describe legionnaire’s disease
- bacteria
- Px
- Transmission
- Ix
- Mx

A

Legionella pneumophilia (gram -ve, bacillus, intracellular).
Signs of pneumonia and AKI (hypoNa, raised Ur/Cr).
Contaminated water - air conditioning, water storage
Can be detected in urine.
Fluoroquinolone (ciprofloxacin) or macrolide (erythromycin)

68
Q

TB drugs and SE

A
  • Rifampicin can cause red secretions (tears, sweat, urine etc.). Rifampicin = Red.
  • Isoniazid can cause fever, jaundice, and nausea. And peripheral neuropathy (PerI- Isoniazid), it causes this by depleting Vitamin B6, so we may co-prescribe Pyridoxine.
  • Pyrazinamide can cause hyperuricaemia (and gout) and hepatotoxicity.
  • Ethambutol can cause optic neuritis / eye symptoms such as colour blindness. Ethambutol = eye.
69
Q

Paraneoplastic features of lung ca

A

Squamous cell: PTHrp, clubbing, HPOA (hypertrophic osteoarthropathy - a syndrome characterized by the triad of periostitis, digital clubbing and painful arthropathy of the large joints, especially involving the lower limbs).

Small cell: ADH, ACTH, hCG, Lambert-Eaton syndrome

70
Q

Describe lung cancer cells

A

95% are bronchial carcinomas
Non-small cell (70-80%)
- Adenocarcinoma (35%) most common lung cancer and associated with asbestos exposure, also most common cell type in non-smokers. From mucus glands.
- Squamous cell carcinoma (25%). From epithelium, most strongly associated with cigarette smoke.
- Large cell (10%) - poor prognosis

Small cell (20-30%) - arise from endocrine Kulchisky cells and secrete hormones.

70
Q

Describe lung cancer cells

A

95% are bronchial carcinomas
Non-small cell (70-80%)
- Adenocarcinoma (35%) most common lung cancer and associated with asbestos exposure, also most common cell type in non-smokers. From mucus glands.
- Squamous cell carcinoma (25%). From epithelium, most strongly associated with cigarette smoke.
- Large cell (10%) - poor prognosis

Small cell (20-30%) - arise from endocrine Kulchisky cells and secrete hormones.

However NB, 2o mets to lung are more common than primary lung tumours (e.g. kidney - RCC).

71
Q

Lung ca Px (local sx), Ix, Mx

A

Px - persistent dry cough, haemoptysis, breathlessness, chest pain. Weight loss.
- May effect brachial plexus = shoulder pain
- Spread to sympathetic ganglion (Horner’s) - ipsilateral ptosis, miosis, anhidrosis
- Left recurrent laryngeal = hoarsness
- Oesophagus dysphagia, heart pericarditis, SVC facial congestion.

CXR, Fine needle biopsy, CT CLA for staging.

71
Q

Lung ca Px (local sx), Ix, Mx

A

Px - persistent dry cough, haemoptysis, breathlessness, chest pain. Weight loss.
- May effect brachial plexus = shoulder pain
- Spread to sympathetic ganglion (Horner’s) - ipsilateral ptosis, miosis, anhidrosis
- Left recurrent laryngeal = hoarsness
- Oesophagus dysphagia, heart pericarditis, SVC facial congestion.

CXR, Fine needle biopsy, CT CLA for staging.

Surgery, chemoradiotherapy.

72
Q

Mesothelioma Ax, Px, Ix, Mx

A

Ax - occupational exposure to asbestos. Long latent period.
Px - dull diffuse chest pain w/ recurrent pleural effusion.
Ix - CXR/CT - thoracoscopy w/ biospy.
Mx - Pemetrexed + cisplatin chemo.

73
Q

GORD Px, Ix, Mx, Cx

A

Retrosternal chest pain - related to meals, worse when lying. Acid brash, odynophagia. can be chronic cough, layngitis.

OGD if red flags (anaemia, weight loss, anorexia, progressive Sx, melaenia/haematemesis, dysphagia)

Conservative - smoking, alcohol, weight, no food before bed.
Medical - PPI (ompeprazole), H2RA (climetidine)
Surgical - Nissen fundoplication.

73
Q

GORD Px, Ix, Mx, Cx

A

Retrosternal chest pain - related to meals, worse when lying. Acid brash, odynophagia. can be chronic cough, layngitis.

OGD if red flags (anaemia, weight loss, anorexia, progressive Sx, melaenia/haematemesis, dysphagia)

Conservative - smoking, alcohol, weight, no food before bed.
Medical - PPI (ompeprazole), H2RA (climetidine)
Surgical - Nissen fundoplication.

Barrett’s -> Oesophageal adenocarcinoma. Stricture.

74
Q

CD, UC - differences.

A

CD has granulomas (non-caseating) and goblet cell numbers increase.’

Smoking is protective in UC.

75
Q

Skin lesions in IBD

A

Erythema nodosum (most common) pyoderma gangrenosum.

76
Q

Ix and Mx in CD

A

pANCA negative always. Bloods, stool calprotectin.
Gold std is colonoscopy/biopsy (granulomas)

1st line - stop smoking.
Induce remission - oral pred, 2nd is 5ASAs. Severe IV hydrocortisone.
Maintenance - azathioprine/mercaptopurine. Can cause thrombocytopenia.

Treat anaemia/malabsorption.

77
Q

UC Ix and Mx
Cx

A

pANCA can be positive.
Colonoscopy w/ biopsy diagnostic.

Flares - topical 5ASAs, then oral. Then steroids if fails (IV if severe)
Remission - 5 ASAs. Severe oral azathioprine or mercaptopurine.

Related to ankylosing spondylitis (HLAB27), autoimmune eye problems. Sclerosing cholangitis.

78
Q

Bowel ca

A

FAP and HNPCC are both AD.

Px w/ colicky abdo pain, weight loss, anaemia, intestinal obstruction.

FIT is first line. DRE. Gold std is colonoscopy w/ biopsy. CEA is tumour marker.

79
Q

Where are diverticula most likely?
Px, Ix, Mx

A

Sigmoid colon (smallest lumen, highest pressure). Low fibre diet is main RF

Px with asymptomatic or LIF pain, constipation, bleeding, palpable mass. Perforation?
Ix - gold std is contrast CT colonography. COLONOSCOPY IS CI IN DIVERTICULITIS.

Tx w/ abx if diverticulitis. Fibres, laxatives/analgesia.

80
Q

Gallstone Tx

A

Analgesia and elective cholecystectomy.

If cholecystitis - cefotaxime, NBM.
Cholangitis is medical emergency requiring sepsis 6, ERCP to remove stone. Only get jaundice with this one.

81
Q

What can you not give in peptic ulcer disease?
Or renal disease

A

NSAIDs, colchicine given instead.

Colchicine cannot be given in renal disease either.