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Year 4 CCC > Primary Care: Chronic conditions > Flashcards

Primary Care: Chronic conditions Flashcards

1
Q

Physiology of Asthma? (x3)

A
  1. Airway inflammation: caused by mast cell + basophil degranulation causing release of inflammatory mediators.
  2. Airway hyper-responsiveness
  3. Airway narrowing: bronchial smooth muscle contraction, further exacerbated by ^mucus production
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2
Q

What does a FeNO (exhaled nitric oxide) test for in asthma?

A

To identify eosinophilic inflammation (particularly in children)
May predict response to monteleukast

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3
Q

Management of Asthma?

  1. Reliever?
  2. Regular preventer?
  3. Step 3 (initial add on)
  4. Step 4 (poor control)
A
  1. Inhaled SABA
  2. Add ICS (400mcgBD)
    (if asthma uncontrolled with SABA alone)
  3. Add LABA +/- ^ICS to 800mcgBD.
    (NICE recommends adding LTRA before LABA)
  4. ^ICS to 2000mcgBD +/- LTRA, theophylline, BA tablet

(can then offer to change ICS+LABA to MART regime w/ low maintenance ICS.

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4
Q

What is uncontrolled asthma defined as?

A

3 or more days/week symptoms
3 or more days/week required use of SABA for sx relief
1 or more nights/week awakening due to asthma

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5
Q

a) SABAs?
b) LABAs?
c) Their MoA?

A

a) Salbutamol, Terbutaline sulfate
b) Salmeterol, Formeterol fumarate
c) MoA: Beta2-receptor Agonists > decrease cAMP in airway smooth muscle > lowers intracellular Ca2+ > resulting in relaxation.

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6
Q

a) ICS examples?
b) MoA?
c) OSCE counsel on steroids.

A

a) Beclomethasone bipropionate, Budesonide.
b) Calm inflamed airways by suppressing action of inflammatory cells + inhibiting release of inflam mediators (histamine/leukotrienes/cytokines).
c) V different to anabolic steroids of bodybuilders. Low dose, goes straight to airways meaning less s/e and less absorbed by rest of body.

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7
Q

Example of LTRA (leukotriene receptor antagonist) , and what is it especially helpful in?

A

Montelukast.
Especially helpful if have hayfever/allergies as well as asthma because during an allergic reaction your body releases leukotrienes.
Very helpful in exericise-induced asthma.

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8
Q

What is MART?

A

Maintenance + Reliever Therapy = ICS + fast acting LABA.
Eg:
Beclomethasone w/ Formoterol
Budesonide w/ Formoterol

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9
Q

What does the Type 1 Diabetic annual review consist of?

A 
HbA1c- target 48mmol/mol
BP- intervene if >135/85
Cholesterol- <4mmol/L
Wt monitoring
Renal function- urine albumin:creatinine (ACR), CKD if ACR>2.5mg/mmol for men, or 3.5mg/mmol for women.
Retinopathy screen
Diabetic foot check
Sexual dysfunction
Screen for depression
Abdominal adiposity at injection sites
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10
Q

What is Hyperosmolar Hyperglycaemic state?

A
  • High blood sugars (30s/40s)
  • Usually precipitated by infection/stroke/trauma/MI
  • May present with: confusion/dehydration/thirst/N&V
  • Absence of ketones
  • Complications: seizures/DIC/rhabdomyolsis
  • Mx: fluids!! (if not better after rehydration, consider fixed rate insulin 0.5 U/kg/hr)
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11
Q

(Diabetes NICE Targets)

If on NO drugs?

A

48mmol/mol (6.5%)

With lifestyle + diet changes.

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12
Q

(Diabetes NICE Targets) If on 1 drug:

a) That doesn’t cause hypos (metformin)
b) That does cause hypos

A

a) 48mmol/mol

b) <53mmol/mol

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13
Q

When would you add a 2nd and 3rd drug for diabetes?

A

2nd drug: if >58mmol/mol
(target then <53mmol/mol)

3rd drug/ or insulin: if STILL >58mmol/mol (target then <53mmol/mol)

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14
Q

What is Charcot foot? (also called Charcot arthropathy)

A

A condition affecting the bones, joints + soft tissues of the foot + ankle, characterized by inflammation in the earliest phase.
Bone destruction, sublaxation, dislocation + deformity (hallmark is ‘rocker-bottom’)

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15
Q

What are 4 types of insulin regime?

A
  1. Once daily (long-acting, given at bedtime. Not for Type 1!)
  2. Twice daily (biphasic insulin)
  3. Basal-bolus (long acting given at bedtime, combined with rapid acting). Most common regime
  4. Continuous subcut insulin infusion (used in pts with recurrent hypos, unpredictable livers + delayed meals.
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16
Q

a) e.g. of a Biguanide?

b) MoA?

A

a) Metformin
b) Decreases gluconeogenesis in liver + ^peripheral utilisation of glucose (only effective if some residual functioning pancreatic islet cells)

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17
Q

a) e.g. of a Sulfonylurea?

b) MoA?

A

a) Gliclazide, Glimepiride

b) Directly ^insulin secretion (so only effective if some residual pancreatic B-cell function)

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18
Q

What are two benefits of metformin?

A
  1. Cardioprotective!

2. Doesnt cause hypos.

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19
Q

Examples of GLP-1 Mimetics and their MoA?

A

Exenatide, Liraglutide.

MoA: Activates GLP-1 to ^insulin pancreatic secretion.

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20
Q

When are GLP-1 Mimetics indicated (because they are expensive)?

A

BMI>35 as causes weight loss by reducing gastric emptying + feel full.

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21
Q

Examples of DPP-4 inhibitors and their MoA?

A

Linagliptin, Sitagliptin, Alogliptin (any -gliptin)

MoA: ^insulin secretion.

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22
Q

Why are DPP-4 inhibitors (-gliptins) good?

A

Few s/e: not excreted by kidneys so can take even if renal impairment.
Dont need to inform DVLA.
Can cause pancreatitis.

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23
Q

Examples of SGLT2 inhibitors and their MoA?

A

Dapagliflozin
Empagliflozin
MoA: inhibition of sodium-glucose transporters reduces glucose re-absorption in the renal tubule.

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24
Q

What is the main s/e of SGLT2 inhibitors?

When are they contraindicated?

A

Urine more sugary- so ^risk of UTIs/thrush.

CI: renal impairment, severe liver disease.

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25
Q

What is 1st line for HTN in a pt with diabetes?

A

ACEi as it protects kidneys. (if afrocarribeans: ACEi AND diuretic/Ca2+-channel blocker)

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26
Q

What would you use in pregnancy for HTN in a pt with diabetes?

A

Calcium-channel blocker

ACEi contraindicated in 2nd/3rd tri due to foetal renal damage

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27
Q

How do you diagnose Diabetic Neuropathy?

A

Persistent albuminuria.
This is measure with urinary ACR on a first-pass morning sample:
>2.5mg/mmol in men is abnormal
>3.5mg/mmol in women is abnormal

If abnormal, repeat within 4months.
Then if abnormal again: ACEi (ramipril 5mg)

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28
Q

Why is there no change in cardiac enzymes in angina?

A

There is ischaemia but no necrosis (the extensive necrosis of cardiac muscle is whats associated with release of cardiac enzymes)

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29
Q

What are the 3 types of angina?

A
  1. Stable: induced by effort, relieved by rest.
  2. Unstable: ^freq + severity, occurs on minimal exertion/at rest. (^ risk MI)
  3. Variant (Prinzmetal’s angina): coronary artery spasm. Pain usually at rest, showing ST elevation. Circadian rhythm (early mornin) (occurs more in younger women)
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30
Q

What is the most important risk factor for an MI?

A

Hypercholesterolaemia!

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31
Q

What 3 proteins do you test for in MI?

A
  1. Troponin T + I (the most sensitive + specific markers of myocardial necrosis)
  2. Creatinine Kinase (CK-MB is sensitive to heart injury)
  3. Myoglobin
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32
Q

Why do you maybe not give oxygen during MI?

A

High flow oxygen can stimulate free radicals which can precipitate another MI (so dont give if sats >95%)

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33
Q

Primary Management of MI?

A 
M(O)NACH
Morphine (+ antiemetic, such as metoclopramide)
Nitrates (GTN + nitroglyceride)
Aspirin 300mg
Clopidogrel 300mg 
Heparin- fondaparinux
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34
Q

Secondary management of MI?

a) Unstable angina and NSTEMI
b) STEMI

A

a) GRACE score to calculate risk of future cardiac event (medium/high risk= coronary angiography/PCI)
b) Emergency restoration of coronary perfusion: primary PCI (stent) and Thrombolysis asap (streptokinase)

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35
Q

Further management of MI (post discharge)?

A

BASIT!

  • Beta-blocker (bisoprolol), if asthmatic use ca-channel blocker, if COPD use metoprolol first then change biso.
  • Aspirin 75mg
  • Statin (atorvastatin 80mg)
  • Inhibitor of ACE (ramipril 10mg)
  • Ticagrelor 90mg BD (for 12months, then just aspirin)
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36
Q

Ticagrelor is better in mx after MI. What is clopidogrel better for?

A

Clopidogrel is better for stroke/TIA/PVD.

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37
Q

What is the classification system for heart failure?

A

New York Heart Association
Class I: no limitations
Class II: slight limitation on physical activity
Class III: marked limitation on physical activity
Class IV: sx of HF are present even at rest

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38
Q

Examples of serum natriuretic peptide, and what are they used to measure?

A

BNP: B-type natruretic peptide

Released into blood when the ventricles are stretched.
BNP>100 = referral/assessment <6wks
BNP>400 = referral/assessment <2wks
BNP<100 = HF is unlikely (consider DDx)

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39
Q

What can BNP also be raised in?

A 
Chronic hypoxaemia
Renal dysfunction
Advanced age
Liver cirrhosis
Sepsis
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40
Q

What is the pneumonic for a CXR for LVF?

A

ABCDE!
A- Alveolar oedema (bat’s wing)
B- Kerley B lines (interstitial oedema- fluid between lung lobes)
C- Cardiomegaly
D- Dilated prominent upper lobe veins
E- Pleural effusion (blunting of costophrenic angles)

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41
Q

(Management of HF)

Diuretics?

A 
Loop Diuretic (Furosemide/ Bumetanide/ Torasemide)
If resistant oedema: + Thiazide diuretic or Spironolactone (K+ sparing)

Monitor: renal function, serum electrolytes (before and 1-2wks after start).

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42
Q

What are some adverse effects of diuretics?

A

Orthostatic HTN, dehydration, renal dysfunction, electrolyre imbalances, hyperuricemia, may precipitate gout.

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43
Q

(Management of HF)

ACEi and monitoring?

A

E.g. Ramipril: start low dose + titrate up according to BP + eGFR.
Monitor: renal function + serum electrolytes before starting, 1-2wks after, then 1-2wks after dose^. Then every 6months.

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44
Q

What is 2nd line to ACEi in HF if pt cannot tolerate chronic cough?

A

Angiotensin-II receptor antagonists: (ARBs)

Candesartan, losartan, valsartan.

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45
Q

When are beta-blockers used in the context of heart failure?

A

1st line (in combo with ACEi!) for HF due to left ventricular systolic dysfunction (LVSD) .
Aim for HR 60bpm
N.b. prescribe both BB and ACEi, but only start one at a time.

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46
Q

How is LVSD defined?

A

It is defined as a left ventricular ejection fraction <40% (moderate/severe systolic dysfunction)

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47
Q

Standard beta-blocker? Which one would you use in elderly?

A

Bisoprolol
Elderly- nebivolol!

Start low, don’t increase when fluid filled.

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48
Q

What does Digoxin do? How do you monitor it?

A

Reduces HR and ^force of contraction.

Monitor for signs of toxicity + renal function. Cardiac adverse effects associated with OD.

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49
Q

What is Enestro?

indication/CI/SE

A

Sacubritil + Valsartan

Indications: symptomatic HF with reduced ejection fraction.
C/I: concomitant use with ACEi.
S/E: Can interact with spironolactone to cause hyperkalaemia (monitor)

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50
Q

What is Ivabradine contraindicated in?

A

AF!!

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51
Q

What to do if severe LVSD on ECHO?

A

Refer for implanted automatic cardiac defibrillator, or pacemaker.

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52
Q

How does Acute Heart Failure present?

A

Dyspnoea, anxiety + tachycardia.

Can eveolve into cardiogenic shock.

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53
Q

How do you treat Acute HF?

A
  • Sit up, 100% O2 flow
  • ECG/FBC/U&Es/Cardiac enzymes/ABG/CXR
  • Sublingual nitrates (enhance myocardial perfusion)
  • IV opiates (reduce anxiety + preload)
  • IV furosemide
  • If systolic >90, IV isosorbide dinitrate
  • If systolic <90, treat as cardiogenic shock.
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54
Q

What are the monitoring parameters whilst on the medications for HF?

A
  • Cr<200umol, or no ^ >50% from baseline
  • K<5.5mmol
  • Systolic BP >100mmHg
  • No symptoms of orthostatic hypotension
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55
Q

Difference in regards to the following of an UMN lesion (stroke) and LMN lesion?

a) Tone
b) Atrophy
c) Fasciculations
d) Reflex
e) Babinski

A

UMN:
Tone- Increased (some initial weakness + stiffness)
Atrophy- Absent (can get some due to lack of use)
Fasc- Absent
Relex- Hyperactive
Babinski- Present (toes up)

LMN:
Tone- Decreased/absent
Atrophy- Present
Fasc- Present
Reflex- Decreased/absent
Babinski- Absent (toes down)
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56
Q

Wernicke’s vs Broca’s dysphasia?

A

Wernicke’s: Receptive (WR)

Brocka’s: Expressive (BE) (think that man in GP)

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57
Q

What is the basis of Rhomberg’s test?

A

Three inputs for balance: Vestibular/cochlear system, Vision, Proprioception.
Need 2/3- when you close eyes, both others must be working for balance.
If Rhomberg +ve: the fall! Which means they have sensory ataxia.
Sign of a posterior circulation (cerebellar) stroke.

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58
Q

Components of ABCD2 score? For assessing the risk of a subsequent stroke after a TIA.
(high risk = 4 or more)

A 
Age>60
BP>140/90
Clinical features: unilateral weakness, speech disturbances.
Duration of symptoms
Diabetes
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59
Q

Management of TIA?

A

TIA nearly always ischaemic + embolic.
So can use antiplatelet asap.
Consider carotid USS: if >70% stenosis at origin of internal carotid, needs endarterectomy within 2wks.

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60
Q

(Acute Stroke Management) When do you need to CT head within 1 hour?

A

a. Indications for thrombolysis (need to exlude haemorrhage)
b. RF for haemorrhagic stroke (on anticoagulants, bleeding tendency, decreased consciousness)
c. Unexplained progressive/ fluctuating sx
d. Meningism
e. Thunderclap headache (SAH)

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61
Q

Management of Ischaemic Stroke? (after haemorrhagic ruled out with CT)

A

a. Thrombolysis (Alteplase)- if started within 4.5hrs of stroke onset. (if later- more cerebral oedema = more likely to have haemorrhagic transformation)
b. Aspirin 300mg (PO/rectal) within 24hrs. PPI if dyspepsia
c. After 2 weeks aspirin, start 75mg Clopidorgrel for life!
d. Statin (48hrs after)
e. Carotid (imaging)
f. Control BP + CVD risk factors

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62
Q

Secondary prevention of Stroke/TIA medications?

A
  1. Clopidogrel 75mg OD (alternative: dipyridamole/ aspirin)
  2. Statin (atorvostatin 40mg)
  3. Antihypertensives
  4. Anticoagulate (only if AF)
  5. Optimise mx of other conditions
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63
Q

What is the commonest risk factor for CKD?

A

Diabetes (diabetic nephropathy)

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64
Q

(Metabolic complications of CKD) Why anaemia and what type?

A

Normocytic anaemia- due to reduced erythrpoietin production.

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65
Q

(Metabolic complications of CKD) Why do people develop bone-mineral disorder?

A 
High PO4 (phosphate retention because of low GFR)
Low serum calcium + high PTH (PTH controlled by -ve feedback of calcium levels in the blood). Low Ca + high PTH= secondary hyperparathyroidism.
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66
Q

Why may CKD result in metabolic acidosis?

A

Due to low serum bicarbonate on venous bloods.

67
Q

Why do you investigate serum urea in CKD?

A

INCREASES with reduced renal excretion due to breakdown of amiino acids.

68
Q

Why may serum urea be disproportionately high/ low?

A

Disproportionately high: catabolic state, high protein intake, GI bleed, glucocorticoids, dehydration, cardiac failure.
Disproportionately low: low protein intake, liver failure.

69
Q

How does serum creatinine change during CKD?

A

INCREASES with reduced renal excretion. Insensitive marker of earlier renal impairment. Production related to muscle mass. (so may be relatively low if elderly/wasting/amputee).

70
Q

How do you manage/monitor CKD in primary care?

A

Anaemia: check haematinics, replace iron/B12/folate.
Acidosis: consider sodium bicarb supplements.
Oedema: consider diuretics, restrict fluid/sodium intake
Restless legs: check ferritin, clonazepam, gabapentin.
Bone disease: Vit D analogues, phosphate control.

71
Q

What are the target BPs for different ACRs in CKD?

A

For ACR <70 = 140/90
For ACR>70 = 135/80

ACR (albumin:creatinine) is measured with spot morning urine sample. The higher the worse, indicates level of proteinuria.

72
Q

Why would you still give an ACEi 1st line in CKD, even though they are excreted renally?

A

Anti-hypertensive!, they have a nephro-protective effect.

(dont give in renal artery stenosis)

Risk of hyperkalaemia! Monitor U&Es baseline + 1wk after.

73
Q

Medications to avoid in CKD?

A 
Digoxin
Iodine
Metformin
Opioids
NSAIDs
Diuretics
Lithium
74
Q

Stage 1 HTN definition?

Stage 2 HTN definition?

A

Stage 1: Clinic BP >140/90, and subsequent ABPM/HBPM average >135/85

Stage 2: Clinic BP >160/100, and subsequent ABPM/HBPM average >150/95

75
Q

What is the definition of severe HTN?

A

Clinic systolic BP >180, or diastolic BP>110

76
Q

What is definition of accelerated HTN?

A

Clinic BP >180/110, with signs of papilloedema and/or retinal haemorrhage (end organ damage).
Refer them for same-day specialist care.

77
Q

What is the biggest risk factor for CVD?

A

Hypertention.

The risk associated with increasing BP is continuous.

78
Q

Stage 1 hypertension and COC?

A

UKMEC criteria 3 means that the risks of COC outweigh the advantages.

79
Q

How do you grade hypertensive retinopathy.

A

Keith-Wagener classification.

Grade 3/4 are diagnostic of malignant HTN.

80
Q

Different effects of following diuretics:

a. Loop
b. Thiazides
c. K+ sparing/ aldosterone antagonists

A

a. Relieve pulmonary oedema from HF.
b. Relieve oedema from HF, + in low doses HTN
c. Used as add-ons, weak on their own

81
Q

How do you manage treatment resistant HTN?

A
  • Consider spironolactone if K+ <4.5mmol, but if not then ^dose of thiazide.
  • Important to monitor U&Es
  • Can also use alpha/beta blockers.
82
Q

Management of Stage 1 HTN?

A

a. Offer Anti-HTN drug to <80yrs with stage 1 and one or more of: target organ damage, established CVD, renal disease, diabetes, QRISK >20%.
b. Promote lifestyle advice, +4wk follow-up + review.

If they are >40yrs but no evidence of above then just offer lifestyle advice.
If <40yrs, then need to seek specialist to evaluate the cause.

83
Q

Management of Stage 2 HTN?

A

<55yrs: ACEi (start low dose, gradually titrate up whilst checking renal function + serum U&Es.) Or ARB.
>55yrs/ Afro-caribbean origin: Calcium-channel blocker

Step 2 is to combine ACEi/ARB with a calcium-channel blocker.

Step 3 is ACEi/ARB + calcium-channel blocker + thiazide-like diuretic.

84
Q

Pathophysiology of AF?

A

The normal regular electrical impulses generated by SAN are overwhelmed by disorganised impulses:
1. Triggers: usually from base of pulmonary veins.
2. Substrate: structural change (e.g. atrial enlargement)
Causes atria to contract rapidly. The AVN responds intermittently, hence irregular ventricular rate.
Therefore blood not moved effectively into vetricles, leading to pooling of blood which ^risk of thrombus formation +reduces CO.

85
Q

(treatment of AF)

Rate control medication?

A
  1. Beta-blocker (CI in asthma/ poss avoid in COPD)
  2. OR rate-limiting Ca-channel blocker (Diltiazem or Verapamil. CI in heart failure)
  3. Digoxin (only in non-paroxysmal AF for sedentary pts, or if in heart failure)
  4. Amiodarone (an antiarrythmatic, used only if others havent worked)
86
Q

(treatment of AF)

If sx persist after rate control, refer to cardiologist. How do you control rhythm?

A
  1. Electrical cardioversion
  2. Pharmacological cardioversion: flecainide 1st line if no IHD, amiodarone if there is.

IF AF started >48hrs ago, need to anti-coagulate 3wks before cardioversion.

87
Q

(treatment of AF)

Anticoagulation treatment?

A

-Vit K antagonist (Warfarin!): requires INR monitoring (2-3). 1st week needs daily bloods, then weekly until stable, then every 3months.
OR: -Novel anticoagulant (NOAC: Rivaroxaban, Dabigatran, Apixaban). Doesnt require INR monitoring. Need bloods before, 6wks then yearly.

88
Q

How do you assess the risks + benefits of anticoagulation?

A

CHA2DS2Vasc score: offer anticoag if >2

HAS-BLED score: 3 or more then high risk of bleeding.

89
Q

What is a genetic condition that predisposes to COPD?

A

Alpha 1 antitrypsin deficiency - WBC begin to harm the lungs and lung deterioration occurs.

90
Q

FEV1/FVC ratio in:
Obstructive disease
Restrictive disease

A 
Obstructive= reduced <0.7
Restrictive= Normal or >80% predicted
91
Q

MRC Dyspnoea Scale?

Grades 1-5 roughly what do they mean?

A

1- No breathlessness except strenuous exercise
2- SOB when walking up slight hill.
3- Walks slower than others due to SOB, has to stop for breath when walking at own pace.
4- Stop for breath after a few mins on level ground.
5- Too breathless to leave house. Breathless when dressing/undressing.

92
Q

What is the BODE index? And what are the 4 components?

A

Used to identify high-risk COPD pts + predict mortality rate.
(%of predicted FEV1, Distance walked, MRC scale, BMI)

93
Q

Describe characteristics of a Pink Puffer?

A

Emphysema- ^alveolar ventilation, near-normal O2 + normal/low CO2.
Breathless, not cyanosed.
Thin/anxious.
May progress to T1 resp failure.

94
Q

Describe characteristics of a Blue Bloater?

A

Bronchitis- decreased alveolar ventilation with low O2 + ^CO2.
Cyanosed but not breathless.
May develop cor pulmonale.
Rely on hypoxic drive to maintain respiratory effort.
T2 resp failure.

95
Q

How do you investigate COPD with spirometry?

A

15-20mins after:

Salbutamol 200mg / Terbutaline 200mg - delivered by a spacer device.

96
Q

Types of oral therapy in COPD?

A
  1. Aminophylline/Theophylline: consider if pt still symptomatic or cant use inhaler devices.
  2. Mucolytic (carbocysteine): consider in pts with chronic productive cough.
  3. Anxiolytic/antidepressant
  4. Nutritional supplements
  5. Prophylactic Abx (azithromycin)
97
Q

Oral corticosteroids for maintenance treatment of COPD?

A

(Don’t prescribe these in primary care.)

If pt on them long term, monitor for osteoporosis + prescribe bisphosphonates if >65yrs.

98
Q

What are the indications by NICE for LTOT?

After you have assessed with 2x ABGs that are three weeks apart

A

a) PaO2 <7.3kPa when stable, OR:

b) PaO2 7.3-8kPa when stable, AND one of: secondary polycythaemia, nocturnal hypoxaemia, peripheral oedema or pulm HTN.

99
Q

What is Sudden Unexplained Death in Epilepsy? (SUDEP)

A

1/1000 epileptics. Risk correlates with freq + severity of seizures (so ensure compliance with meds).
Alcohol may increase risk.

100
Q

Anti-epileptic drugs and seizure type?

a. Focal
b. Absence
c. Tonic-clonic
d. Myoclonic
e. Tonic/atonic

A

a. Focal: Carbamazepine/ Lamotrigine
b. Absence: Sodium valp / Ethosuximide
c. Tonic-clonic: Socium valp / lamotrigine
d. Myoclonic: Sodium valp (avoid carbamazepine)
e. Tonic/atonic: Sodium valp (avoid carbamazepine)

101
Q

DVLA rules for seizures?

A

1st unprovoked seizure: drive after 6months seizure-free.
Epileptic seizure: drive after 12months seizure-free.

It is pt’s legal responsibility to inform DVLA.

102
Q

What epilepsy drugs increase the risk of osteoporosis?

A

-If on carbamazepine/ phenytoin/ socium valp: this ^risk of osteoporosis. So offer diet advice/ calcium/ vit D supplements.

103
Q

Contraception and epilepsy drugs?

A

Lamotrigine- the only one that doesn’t cause teratogenity.
Also lamotrigine is the only one that doesn’t affect CYP450 (however the oestrogen in COCP reduces lamotrigine, so ^risk of seizure!)

104
Q

Physiology behind MS?

A

A demyelinating disease in which the myelin sheath is damages. This slows/blocks signals to/from brain leading to movement/sensation problems.
Caused by a T-cell mediated autoimmune response.
Demyelination heals incompletely, causing the relapsing-remitting sx.

105
Q

How can you use CSF to investigate MS?

A

Oligoclonal bands of IgG not present in serum suggests CNS inflammation.
MOG + MBP antbodies in those with a single MS-like lesion can preduct time to conversion to definite MS.

106
Q

Management of MS relapse?

A

Methylprednisolone 1g OD IV/PO for 3days (shortens relapse, consider gastroprotection such as ranitidine/omeprazole)

Exclude UTI as cause of exacerbation before steroids started!

107
Q

Management of MS? (disease modifying therapy)

A

Interferon beta: decreases active relapsing-remitting disorders.
Monoclonal antibodies (Natalizumab): reduces relapses + MRI lesions.
Vit D

108
Q

What are the 3 components of Charcot’s Neurologic Triad?

A
  1. Dysarthria (due to plaques in brainstem, interfering with conscious/unconscious movements)
  2. Nystagmus (due to plaques in nerves of eye: Loss of vision, optic neuritis, pain + double vision)
  3. Intention tremor (plaques along motor pathways: tremors, muscle weakness, ataxia, paralysis)
109
Q

What is motor neurone disease?

A

Degenerative condition that affects both upper + lower motor neurons.
Rapidly progressing + fatal. (median survival 2-4 years)

110
Q

What gene is the familial form of MND from?

A

Mutation to superoxide dismutase-1 gene.

111
Q

Presentation of MND?

A
  1. Limb onset (most common): weakness, stiffness, cramping (usually upper limbs), pt may drop things.
  2. Bulbar onset (20%): first sign usually slurred speech due to impaired tongue movement. Coughing fits.
  3. Respiratory onset: dyspnoea + orthopnoea.
112
Q

Non-drug management of MND?

A

Mainstay of treatment is supporting pt + family.

  • PT (clear pulm secretions), OT, SALT.
  • PEG/NG tube consider
113
Q

Drug management of MND?

A
  • Riluzole (neuroprotective glutamate-release inhibitor) may prolong life 2-4months.
  • Hyoscine hydrobromide- excess secretions
  • Diazepam/Baclofen- muscle cramps
  • Antidepressants
  • Analgesics
114
Q

Physiology of Parkinson’s disease?

A

Degeneration of dopaminergic neruons in the substantia nigra (of basal ganglia), which causes decrease in striatal dopamine levels.
Can see Lewy Bodies in affected basal ganglia.

115
Q

What genes may be linked to Parkinson’s disease?

A

PINK1, PARKIN, alpha synuclein

116
Q

Classic triad of Parkinson’s disease?

A
  1. Tremor: ‘pill-rolling’, worse at rest
  2. Rigidity: ^tone. Superimposed tremor causes cogwheel rigidity
  3. Bradykinesia/hypokinesia: slow movement initiation with progressive reduction in speed + amplitude of repetitive actions.

One distinguishing feature!!= does NOT produce weakness!!!

117
Q

How is drug-induced parkinsonism caused?

A

By drugs that block dopamine receptors/ reduce dopamine storage. (e.g. antipsychotics: metoclopramide)

118
Q

What is the gait described as in Parkinson’s disease?

A

Festinant: short shuffling steps with trunk flexed forwards, reduced arm swing, freezing at obstacles, reduced turning speed.

119
Q

How does Levodopa work? (mx for Parkinson’s)

A

(Sinemet, Madopar)
Most effective for controlling sx, esp motor disability.
Levodopa (precursor or dopamine) can cross the BBB, whereas dopamine cannot.
It is given with carbidopa (peripheral DOPA decarboxylase inhibitor) to prevent early conversion to dopamine.

120
Q

Other than Levodopa, what other drugs are used in the management of Parkinson’s?

A
  • Oral/Transdermal dopamine agonists (pramipexole, bromocriptine, cabergoline): initial mx in younger pts.
  • Amantadine (antiviral that stimulates dopamine production)
  • Monoamine-oxidase-B inhibitos (MOA-Bis) (selegiline, rasagiline): prevents breakdown of dopamine in brain.
  • COMT inhibitors (entacapone): inhibit breakdown of dopamine.
121
Q

What is amantadine?

A

Antiviral that stimulates dopamine production. (for Parkinson’s)

122
Q

What are some investigations for RA?

A
  • Rheumatoid factor (RhF): +ve in 70%, also raised in other inflam diseases.
  • Anti-cyclic citrullinated peptide antibodies (ACPA): more specific!
  • FBC: normocytic, normochromic anaemia. Reactive thrombocytosis.
  • ESR/CRP: may be raised (inflam)
123
Q

Management of RA?

A
  • Analgesia
  • Disease-modifying anti-rheumatic drugs (DMARDS): Methotrexate (monitor FBCs + LFTs)
  • TNF inhibitors: Infliximab. Only use if inadequate response to 2 DMARDs.
  • Steroids: pred
124
Q

Red Flag Symptoms in pts with back pain?

A
  • AGED <20 OR >55
  • NOCTURNAL PAIN/ CONSTANT PAIN
  • FEVER, NIGHT SWEATS, WT LOSS
  • NEUROLOGICAL DEFICIT - WEAKNESS, SENSORY LOSS
  • URINARY RETENTION, FAECAL OR URINARY INCONTINENCE
  • TRAUMA
  • THORACIC BACK PAIN
  • SADDLE ANASETHESIA, LOSS OF ANAL TONE
125
Q

What are some common causes of back pain in the following:

a) 15-30yrs
b) 30-50yrs
c) >50yrs

A

a) prolapsed disc, trauma, pregnancy.
b) degenerative spinal disease, prolapsed disc, malignancy.
c) degenerative, osteoporotic vertebral collapse, malignancy, myeloma, spinal stenosis.

126
Q

What is bronchiectasis?

A

Obstructive!

Permanent dilation + thickening of airways. Can be limited to one area of lung, or widespread.

127
Q

Causes of bronchiectasis?

A
  1. Previous severe LRTI (most common cause)
  2. Foreign body aspiration
  3. Disorders of mucocilliary clearance (CF)
128
Q

Management of bronchiectasis?

A

Basis of management is to prevent/slow further deterioration!
Lifestyle advice, PT, Abx for acute exacerbations, mucolytics/saline nebs.

129
Q

What is sometimes forgotten in the mx of respiratory conditions?

A

A long term cough can cause bladder incontinence.

May need bladder retraining, pelvic floor exercises, etc.

130
Q

What is Pulmonary Fibrosis characterised by?

A

SOB
Diffuse infiltrates on CXR
Inflammation/fibrosis on biopsy

131
Q

What are some (non-medication) causes of Pulmonary Fibrosis?

A
  • Idiopathic (most common interstitial lung disease)
  • Occupational: asbestos, coal dust, silica
  • Extrinsic allergic alveolitis: farmer’s + pigeon fancier’s lung
  • Connective tissue diseases: RA, SLE, Sjogren’s syndrome
132
Q

What are some medications that can cause Pulmonary Fibrosis?

A

Amiodarone
Nitrofurantoin
Bleomycin

133
Q

What are some medical managements of Pulmonary Fibrosis?

A
  • Pirfenidone (anti-fibrolytic)
  • Nintedanib (tyrosine kinase inhibitor: anti-fibrolytic)
  • Corticosteroids: for acute exacerbations
  • PPIs: consider as GOR can make sx worse.
134
Q

What are diverticula, and where in the GI tract are they most common?

A
  • Mucosal pouches that push through the muscular wall of the colon.
  • Throughout GI tract, most common in sigmoid + descending colon.
135
Q

What is the difference between:

1) Diverticulosis
2) Diverticular disease
3) Diverticulitis

A

1) Dicerticula present but without sx (70%)
2) Diverticula cause intermittent lower abdo pain, without inflam/infection.
3) Diverticula become inflamed/ infected causing marked lower abdo pain/ fever/ sometimes large rectal bleed.

136
Q

How do you diagnose diverticulosis?

A

Mostly asx, remain undiagnosed.
May present with a large, painless rectal bleed.
Frequent/small/continual bleeds are UNLIKELY to be caused by diverticulitis + require ix!!!

137
Q

How do you diagnose diverticular disease?

A

Characteristic signs+sx:

  1. Intermittent lower abdo pain (usually loeft lower quadrant. Pain may be brought on by eating + relieved by passing stool)
  2. Constipation/ diarrhoea/ occasional large rectal bleeds.
  3. Bloating or passage of mucus rectally

To confirm: barium enema, colonoscopy, or CT colonogram.

138
Q

How do you diagnose diverticulitis?

A

Characteristic signs+sx:

  1. Constant, severe abdo pain usually start in hypogastrium before localising to left iliac fossa)
  2. Fever
  3. Constipation/ diarrhoea/ large rectal bleeds.
  4. Dysuria + urinary frequency
  5. Abscess formation + peritonitis
139
Q

Management of diverticulosis?

A

Asymptomatic that is identified incidentally, doesn’t require further diagnostic evaluation.
Can advise high fibre diet (reduce risk of developing symptomatic diverticular disease)

140
Q

Management of diverticula disease?

A
  • High fibre diet

- Paracetamol (avoid NSAIDs / Opioids- as they ^risk of diverticular perf)

141
Q

Management of diverticulitis?

A

Mild/uncomplicated can be managed at home:

  • Broad spec abx (co-amox, or cipro+metronidazole)
  • Paracetamol
  • Clear liquids only, gradually reintroduce solids as sx improve.

If needing admission:
Pethidine ! (opioid) for pain whilst waiting.

142
Q

What are some genes that may be involved in the development of Crohn’s?

A

NOD2, CARD15

143
Q

Where does Crohn’s especially affect in the gut?

A

Terminal ileum + proximal colon.

144
Q

Histology of UC vs Crohns?

A

UC: Hyperaemic/haemorrhagic granular colonic mucosa + pseudopolyps formed by inflammation.
Crohn’s: Transmural granulomatous inflam, resulting in gut stenosis + penetrating ulcers leading to abscesses + fistulae.

145
Q

What is a Isotretinoin?

A

A medication used to treat acne- now a RISK FACTOR for IBD!!!

146
Q

What is the appearance of Crohn’s and UC on a colonoscopy/sigmoidoscopy?

A

UC: colon wall is thinner + shows continuous inflammation.

Crohn’s: Colon thickened, cobblestone appearance.

147
Q

What are some extraintestinal signs in UC?

A
  • Clubbing
  • Erythema nodosum
  • Conjunctivitis/ Episcleritis
  • Ankylosing spondylitis
  • Fatty liver
148
Q

What is the Trueloe-Witts criteria?

A

Used to assess the severity of UC!

  • Stool freq
  • Temp
  • Pulse
  • Haemoglobin
  • ESR
149
Q

Management of:

a) Mild/Moderate UC (<6 motions)
b) Severe UC (>6motions + unwell)

A

a) 5-ASA (aminosalicylates: sulfasalazine or mesalazine)
Steroids PR
b) Admit for NBM + IV hydration
IV + PR Steroids

150
Q

What is azathioprine?

A

Immunosuppressive medication for UC/Crohn’s

151
Q

Management of Crohn’s:

a) Mild attacks (symptomatic but systemically well)
b) Severe attacks

A

a) Oral steroid (e.g. pred)
b) Admit for IV steroids
NBM + IV fluids
Treat rectal disease with PR steroids
Metronidazole PO can help

152
Q

(NICE) When do you suspect NAFLD? (non-alcoholic fatty liver disease)

A
  • Risk factors for metabolic syndrome
  • Persistent LFT elecation for >3months (usually ALT is 3xnormal + exceeds AST)
  • Upper abdo USS consistent with fatty liver changes

(DONT use routine LFTs to rule out NAFLD as may be normal!)

153
Q

What are some inherited causes of Chronic Liver Disease?

A
  • Alpha-1 antitrypsin
  • CF
  • Wilson’s disease (copper)
  • Haemochromatosis (iron)
154
Q

Pathophysiology of Hepatic Encephalopathy?

A
  • Toxins that the liver usually filters out build up in blood + may enter brain (ammonia)
  • Can be triggered by dehydration/ infection.
  • Medication is aimed at preventing growth of bacteria that produce ammonia in the gut: Lactulose, Neomycin, Rifaximin.
155
Q

Investigating for auto-antibodies in liver disease:

a) Autoimmune hepatitis
b) Primary biliary cirrhosis

A

a) High titres of anti-nuclear antibodies (ANA) + anti-smooth muscle antibodies (ASMA)
b) High titres of anti-mitochondrial antibodies (AMA)

156
Q

What does serum caeruloplasmin test for?

A

Wilson’s disease

157
Q

Management for Chronic Liver disease?

A
  • Advice (decrease salt, alcohol + smoking)
  • Vit K 10mg (help with clotting)
  • Remove causes (medication or alcohol)
  • Diuretics for ascites
  • Liver transplant
  • Liver USS every 6/12 to check for HCC
158
Q

Pathophysiology of Coeliac Disease?

A
  1. Upon exposure to Gliadin, the enzyme tissue transglutaminase modifies the protein + through a T-cell mediated autoimmune response it cross-reacts with the small bowl tissue
  2. This causes an inflammatory reaction, leading to villous atrophy.
159
Q

What are two risk factors for Coeliac disease?

A
  • HLA: types HLA-DQ2 (90%), or HLA-DQ8

- Dermatitis herpatiformis: autoimmune blisterisng skin condition associated w/coeliac disease.

160
Q

What antibodies are you investigating for in Coeliac disease?

A

Alpha-gliadin
Transglutaminase
Anti-endomysial

161
Q

Steroid management for Eczema?

A

Mild: 1% hydrocortisone

Moderate: betamethasone 0.1% (Dermovate) - highly potent, not used on face/genitals.

S/e: skin thinning, striae formation, telangesctasia, adrenal suppression.

162
Q

Presentation of guttate psoriasis?

A

Transient psoriatic rash, frequently triggered by strep infection.
Multiple red, teardrop lesions.

163
Q

Management of psoriasis?

A

Regular emollients!

1st line: (up to 4wks initially)
Potent corticosteroids
Vit D analogue OD (calipotriol/calcitriol- reduces cell division)
2nd line: (if no improvement after 8wks)
Vit D analogue BD
SHort action dithranol
3rd line: 
Potent corticosteroid BD (4wks)
Coal tar

Year 4 CCC (2 decks)

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