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1
Q

Causes of microcytic anaemia?

A

TAILS
Thalassaemia, anaemia of chronic disease, iron deficiency, lead poisoning, sideroblastic anaemia (X-linked)

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2
Q

What MCV is classified as microcytic anaemia?

A

<80 femtolitres

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3
Q

What MCV is classified as normocytic anaemia?

A

80-100 femtolitres

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4
Q

What MCV is classified as macrocytic anaemia?

A

> 100 femtolitres

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5
Q

Causes of normocytic anaemia?

A

[3x As, 2x Hs]

  • Acute blood loss
  • Haemolytic anaemia - i.e. sickle cell disease
  • Anaemia of chronic disease
  • Aplastic anaemia - temp. stopped RBC production (bone marrow disorder)
  • Hypothyroidism
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6
Q

Causes of macrocytic anaemia?

A
  • MEGALOBLASTIC (B12 deficiency + folate deficiency)
  • NORMOBLASTIC (alcohol abuse, drugs like MTX, liver disease or reticulocytosis)
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7
Q

Direct Coombs test positive?

A

Autoimmune haemolytic anaemia(not in other types of haemolytic anaemia) - can either be warm AIHA or cold AIHA

Warm AIHA is more common

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8
Q

What anaemia can prosthetic valves cause?

A

Turbulent flow around the prosthetic valve = shearing of RBCs.
The valve churns up the cells, and they break down.

=> normocytic haemolytic anaemia

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9
Q

Key findings in G6PD deficiency?

A

X-linked recessive (mainly males)

Acute episodes of haemolytic anaemia; triggered byinfections,drugs(i.e. anti-malarials) orfava (broad) beans.

⇒ jaundice, anaemia, splenomegaly
=> Heinz bodies on blood film

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10
Q

What is pernicious anaemia?

A

Autoantibodies against parietal cells or intrinsic factor.
=> lack absorption of vit B12

Presents with peripheral neuropathy & megaloblastic macrocytic anaemia

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11
Q

What to treat first when we have both B12 and folate deficiency?

A

It is essential to treat theB12 deficiency first, before correcting the folate deficiency.

Giving patientsfolic acid when they have aB12 deficiencycan lead tosubacute combined degeneration of the cord, with demyelination in the spinal cord and severe neurological problems.

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12
Q

Treatment for polycystic kidney disease?

A
  • Tolvaptan (vasopressin receptor antagonist)
  • Antihypertensives (ACE inhibitors)
  • Analgesia
  • Antibiotics for infections (e.g., UTIs or cyst infections)
  • Drainageof symptomatic can be performed by aspiration or surgery
  • Dialysisfor end-stage renal failure
  • Renal transplantfor end-stage renal failure
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13
Q

Chlamydia treatment?

A

First line: doxycycline 100mg twice a day for 7 days

In pregnancy + breastfeeding:
Azithromycin 1g stat, then 500mg OD for 2 days

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14
Q

Gonorrhoea treatment?

A
  • IM ceftriaxone1g - if sensitivities are NOT known
  • ORAL ciprofloxacin500mg - if sensitivities ARE known

=> TEST OF CURE!! with NAAT testing if they are asymptomatic, or cultures if symptomatic

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15
Q

Syphilis treatment?

A

IMdose ofbenzathine benzylpenicillin

Ceftriaxone, amoxicillin and doxycycline are alternatives.

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16
Q

What cancer metastases can cause “cannonball metastases” in the lungs?

A

Metastatic renal cell carcinoma.
These appear as clearly-defined circular opacities scattered throughout the lung fields on a chest x-ray.

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17
Q

A 65 year old male reports significant weight loss as well severe pain in his right loin over the last 4 months which is abnormal for him. He is afrebrile but reports visible clots in his urine. CXR reveal cannon ball cancer metastases in his lungs. What genetic condition predisposes him the most to developing his primary cancer?

A

Primary cancer - renal cell carcinoma
Genetic condition - Von-Hippel Lindau syndrome

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18
Q

UTI treatment in pregnancy?

A
  • Cefalexin
  • Nitrofurantoin (avoid in the third trimester)
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19
Q

Why should trimethoprim be avoided in pregnancy?

A

Folate antagonist. Folate is essential in early pregnancy for normal development. Trimethoprim in early pregnancy can causecongenital malformations, particularlyneural tube defects(spina bifida)

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20
Q

UTI treatment for lower UTI in women?

A

Women = uncomplicated
3 days of oral trimethoprim or nitrofurantoin

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21
Q

UTI treatment for lower UTI in men?

A

Men = complicated
7 days - oral trimethoprim or nitrofurantoin

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22
Q

UTI treatment for upper UTI? men, vs pregnant women?

A

1st line - cefalexin + co-amoxiclav (7-10 days)

Pregnancy - cefalexin is first-line oral, and cefuroxime is first-line IV.

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23
Q

Secondary prevention for stable angina?

A

4x As
- Aspirin (anti-platelet)
- Atenolol (b blocker)
- Atorvostatin
- ACE inhibitor (ramipril)

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24
Q

Interventions for late stage stable angina?

A
  • PCI - percutaneous coronary intervention - insert balloon, then leave stent in place (through femoral or brachial artery)
  • CABG - coronary artery bypass graft - for really severely stenosed coronary arteries - take graft pain from leg, use it to bypass the stenosis in the coronary artery.
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25
Q

Location of two scars from CABG?

A
  • Midline sternotomy
  • Scar on inner calf (harvest the great saphenous vein)
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26
Q

Investigations for angina?

A
  • CT coronary angiography (gold standard)
  • ECG
  • TFTs??
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27
Q

Two types of left-sided heart failure?

A
  • Systolic - reduced ejection fraction (reduced contraction)
  • Diastolic - preserved ejection fraction (stiff muscle, so cannot relax)
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28
Q

Cor pulmonale?

A

Right-sided heart failurecaused byrespiratory disease, ie:

  • COPD (most common cause)
  • Pulmonary embolism
  • Interstitial lung disease
  • Cystic fibrosis
  • Primary pulmonary hypertension
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29
Q

Medical management for chronic heart failure?

A

ABAL:

ACE inhibitor
Beta-blocker (bisprolol)
Aldosterone antagonist (spironolactone)
Loop diuretic (furosemide)

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30
Q

Features of atrial stenosis?

A
  • ejection systolic murmur (crescendo decrescendo|)
  • narrow pulse pressure
  • slow rising carotid pulse
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31
Q

Features of atrial regurgitation?

A
  • diastolic, soft murmur
  • wide pulse pressure
  • collapsing pulse (water hammer pulse)
  • austin flint murmur
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32
Q

Features of mitral stenosis?

A

Loud S1
Mid-diastolic murmur
=> RHEUMATIC FEVER

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33
Q

Features of mitral regurgitation?

A

Pansystolic high pitched murmur
=> congestive HF
=> oedema

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34
Q

Surgical interventions for aortic aneurysm?

A
  • EVAR - endovascular aortic repair
  • open surgery (preferred by NICE)
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35
Q

Definition of abdominal aortic aneurysm? AAA

A

Dilation of abdominal aorta >3cm

Degradation of all 3 layers of the vessels (intima, media and adventitia).

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36
Q

True AAA vs psuedo (false) aneurysm?

A

Degradation of all 3 aortic layers is referred to as a true aneurysm, whilst degradation of less than 3 is a pseudoaneurysm

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37
Q

Definition of aortic dissection?

A

Where the blood enters between the intima and media layers of the aorta

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38
Q

Risk factors for aortic aneurysm + aortic dissection?

A
  • Marfan syndrome and other connective tissue disorders
  • Men
  • Increased age
  • Smoking
  • Hypertension
  • Family history
  • Existing cardiovascular disease
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39
Q

Management for aortic aneurysm over 5.5cm dilation?

A

Elective surgery to prevent rupture:
- open surgery
- EVAR (endovascular aortic repair)

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40
Q

Management for RUPTURED aortic aneurysm? (+ define)

A

Aneurysm rupture = tear of all aortic wall layers (more severe than aortic dissection, which is just inner wall)

  • ABCDE
  • Fluid resuscitaiton
  • URGENT SURGICAL REPAIR (open surgery preferred) - repair with graft
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41
Q

Presentation of ruptured THORACIC aortic aneurysm?

A
  • severe chest pain
  • haemodynamic instability (hypotension + tachycardia)
  • collapse
  • death
  • Cardiac tamponade (due to bleeding into pericardial cavity)
  • Haemoptysis (bleed into airways)
  • Haematemesis (bleed into oesophagus)
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42
Q

Monitoring requirments for AAA?

A

<3 (normal- not AAA)

3-4.4 cm = yearly
4.5-5.4cm = 3 monthly

> 5.5cm (elective surgery)

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43
Q

Cullen’s sign and Grey Turners? where is this seen?

A
  • Rupture of an aortic aneurysm
  • Haemorrhagic pancreatitis (severe)
  • Ruptured ectopic pregnancy
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44
Q

Define: aortic dissection

A

Tear in the innermost layer of aortic wall (intima).
Blood collects between intima and media layers => forms an intramural ‘false lumen’

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45
Q

Most common site for aortic dissection?

A

Right lateral area of ascending aorta
This is area of highest pressure

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46
Q

Management of aortic dissection? (type A vs type B)

A
  • MORPHINE FOR PAIN
  • IV LABETOLOL (to reduce tachycardia)

Type A - (first part of asc aorta) = surgical - aortic graft (EVAR)

Type B - (descending aorta) = normally conservative management with BP control - may also need EVAR

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47
Q

Complications of aortic dissection?

A
  • Cardiac tamponade
  • Myocardial infarction
  • Stroke
  • Paraplegia (motor or sensory impairment in the legs)
  • Aortic valve regurgitation
  • Death
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48
Q

ECG changes in pericarditis?

A
  • Saddle-shaped ST-elevation
  • PR depression
  • No reciprocal ST depression
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49
Q

Investigations in pericarditis?

A
  • ECG
  • Echo
  • Bloods
  • Inflamm markers (high ESR, CRP, WCC)
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50
Q

Management of pericarditis?

A
  • NSAIDs
  • Colchicine (used longer term, 3 mnths, to reduce risk of recurrence)
  • Pericardiocentesis may be required to remove fluid from around the heart if there is a significant pericardial effusion or tamponade.
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51
Q

Diagnosis of peripheral vasc disease? (investigations)

A
  • ABPI (ankle-brachial pressure index) - <0.9
  • GOLD STANDARD = CT angiography (CT or MRI)
  • Duplex doppler ultrasound imaging (speed and volume of blood flow)
  • Buerger’s test - patient lies flat, raise legs to 45 degree angle for 1 min. Positive result if legs goes pallor and then re-perfuses when dropped.
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52
Q

Presentation of peripheral vascular disease?

A
  • 6x Ps
  • Low ABPI (<0.9)
  • Leg ulcers
  • Xanthomata (yellow cholesterol deposits in skin)
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53
Q

What are the 6 Ps of acute limb-threatening ischaemia?

A

Pulseless
Pallor
Pain
Perishingly cold
Paralysis
Paraesthesia

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54
Q

Treatment - for intermittent claudication

A
  • Graded-exercise therapy’, diet control and smoking cessation.
  • STATINS
  • ANTI-PLATELETS - clopidogrel
  • Naftidrofuryl oxalate (5-HT2 receptor antagonist that acts as a peripheral vasodilator)
  • Endovascular angioplasty with stenting
  • Endartectomy
  • Bypass surgery
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55
Q

Treatment - for acute limb-threatening ischaemia?

A

THROMBUS = SURGICAL EMERGENCY

  • revascularisation is needed within 4-6 hours or else amputation risk is increased.
  • Endovascular thrombolysis - use catheter and insert thrombolysis directly into the clot
  • Endovascular thrombectomy - use catheter to remove thrombus
  • Surgical thrombectomy - cut open vessel to remove thrombus
  • Endartectomy
  • Bypass surgery
  • Amputation
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56
Q

Tetralogy of fallot?

A
  • VSD
  • Overriding aorta - lies towwards RHS, meaning deoxy blood can go through VSD and enter aorta!
  • Pulmonary valve stenosis (encourages blood to flow across VSD instead)
    => right ventricle hypertrophy

=> right to left shunt = cyanosis!

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57
Q

Eisenmenger Syndrome?

A

When there is a VSD, blood typically flows from left to right = therefore no cyanosis occurs.

= overtime this leads to right heart overload = RV hypertrophy = higher pressures in RV than LV
= shunt swaps to become RIGHT TO LEFT SHUNT

= NOW IS CYANOTIC (Eisenmenger Syndrome)

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58
Q

Beck’s triad of acute pericarditis?

A

Hypotension
Raised JVP
Muffled heart sounds
=> sign of cardiac tamponade

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59
Q

Important differential for symptoms of meningism?

A

Subarachnoid haemorrhage

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60
Q

Community treatment of meningitis?

A

IM benzylpenicillin (in presence of non-blanching rash)

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61
Q

Prophylactic treatment for meningitis close contacts? time frame of contact?

A

Last 7 days
Single dose of ciprofloxacin

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62
Q

Hospital treatment of bacterial meningitis?

A

ANTIBIOTIC + DEXAMETHASONE:

<3 months - cefotaxime
>3 months - ceftriaxone
(3rd gen cephalosporins)

Dexamethasone - to reduce risk of hearing loss or neurological damage

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63
Q

Kernig’s test?

A

lying the patient on their back, flexing one hip and knee to 90 degrees and then slowly straightening the knee whilst keeping the hip flexed at 90 degrees. This creates a slight stretch in the meninges. Where there is meningitis it will produce spinal pain or resistance to movement.

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64
Q

Brudzinski’s test?

A

lying the patient flat on their back and gently using your hands to lift their head and neck off the bed and flex their chin to their chest. In a positive test this causes the patient to involuntarily flex their hips and knees.

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65
Q

Difference between CSF lumbar puncture in viral vs bacterial meningitis?

A

Bacterial - yellow/cloudy (viral - clear)
Bacterial - low glucose (bact. use up)
Bacterial - high protein (bact. produce)
WCC - high neutrophils (bacterial) vs high lymphocytes (viral)

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66
Q

What does purpuric non-blanching rash indicate?

A

DIC caused by meningococcal septicaemia (N.meningitidis has entered blood stream)

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67
Q

Why might we add amoxicillin on top of ceftriaxone in meningitis?

A

If there is a high risk of listeriosis (i.e. older age 73yo).
AMOXICILLIN - to cover listeria

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68
Q

Murphy’s sign? When is it positive?

A

Positive in acute cholecystitis

Press in upper RQ
Patient inhales deeply
Gallbladder will move downwards; when it comes into contact with your hand the patient will STOP inhaling
(due to acute pain)

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69
Q

Investigation for acute cholecystitis + findings?

A

Ultrasound
- Thick-walled gallbladder
- Stones in gallbladder
- Fluid around the gallbladder

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70
Q

Investigation for acute cholangitis + findings?

A
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71
Q

Charcot’s triad + which condition?

A

Acute cholangitis presents with Charcot’s triad:

Right upper quadrant pain
Fever
Jaundice (raised bilirubin)

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72
Q

Management of acute cholangitis?

A
  • IV ANTIBIOTICS (due to infection - risk of sepsis)
  • ERCP - to remove gallstones, or baloon dilatation or stents for strictures
  • Laparoscopic cholecystectomy (remove gallbladder) - once stable
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73
Q

Management of acute cholecystitis?

A
  • IV ANTIBIOTICS
  • ERCP to remove gallstones if stuck in common bile duct
  • Laparoscopic Cholecystectomy (removal of the gallbladder) is usually be performed during the acute admission, within 72 hours of symptoms
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74
Q

Wilsons disease? typical patient + presentation?

A

Excess copper in all tissues, particularly in liver
Typically younger patient

  • Kayser-fleischer rings (cornea)
  • Chronic hepatitis - leads to liver cirrhosis
  • Neurological symptoms - tremor, dysarthria (speech difficulties) and dystonia (abnormal muscle tone) + Parkinsonism (copper in basal ganglia)
  • Psychiatric symptoms - abnormal behaviour,depression,cognitive impairment andpsychosis
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75
Q

Treatment for pruritis?

A

Cholestyramine (bile acid sequestrant)

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76
Q

What is hepatic encephalopathy + exam finding?

A

Reversible syndrome in advanced liver dysfunction.

Results from accumulation of neurotoxic substances in the brain = AMMONIA

ASTERIXIS (sign of grade 2/3 HE) - patient told to hold hand like stopping traffic, but it flaps down instead

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77
Q

Drug to treat hepatic encephalopathy?

A

Lactulose (first-line) - laxative to promote ammonia excretion

Rifaximin - antibiotic

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78
Q

Epigastric pain radiating to the back?

A

Acute pancreatitis

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79
Q

AST:ALT ratio in NAFLD?

A

Higher ALT (reversed ratio)

> 0.8 indicates advanced fibrosis

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80
Q

AST:ALT ratio in ALD?

A

> 1.5 (high AST!)
(2:1 ratio)

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81
Q

Cushing’s reflex/triad?

A

Hypertension + bradycardia + irregular respirations

This is the response to raised ICP
- in extradural haemorrhage
- in head injury
etc

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82
Q

First line treatment for trigeminal neuralgia?

A

This is headache with trigeminal nerve distribution.

  • Carbamazepine (anti-spasmodic)
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83
Q

Hepatic encephalopathy?

A

Excess ammonia
reversible syndrome
COMPLICATION of advanced CIRRHOSIS
++ ASTERIXIS - hand flap (grade 2/3)

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84
Q

Treatment for hepatic encephalopathy?

A

IV lactulose (laxative) - to exrete excess ammonia
Rifaximin - antibiotic (to reduce int. bacteria producing ammonia)

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85
Q

Child Pugh score use? components?

A

severity of cirrhosis
A–Albumin
- B–Bilirubin
- C–Clotting (INR)
- D–Dilation (ascites)
- E–**Encephalopathy

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86
Q

Scan used in cirrhosis?

A

Transient Elastography (FibroScan)

Used to assess the stiffness of the liver using high-frequency sound waves. It helps determine the degree offibrosis(scarring) to test forlivercirrhosis.

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87
Q

Wernicke’s encephalopathy vs Korsakoff syndrome

A

Both caused by thiamine / VITAMIN B1 deficiency
Wernicke’s encephalopathy represents the “acute” phase of the disorder and Korsakoff’s amnesic syndrome represents the disorder progressing to a “chronic” or long-lasting stage.

Wernicke’s encephalopathyis a medical emergency with a high mortality rate.

Korsakoff syndromeis often irreversible and results in patients requiring full-time or institutional care.

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88
Q

Triad of symptoms in Wernicke’s encephalopathy?

A

Confusion
Oculomotor disturbances (eye muscle paralysis)
Ataxia (difficulties with coordinated movements)

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89
Q

Features of Korsakoff syndrome include?

A

Memory impairment (retrograde and anterograde)
Behavioural changes

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90
Q

Causes of Wernicke’s encephalopathy?

A

Mainly EXCESS ALCOHOL

But also:
- Pancreatitis
- Liver dysfunction
- Vomiting / hyperemesis gravidarum
- Starvation/fasting
- Cancer
- AIDS

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91
Q

Medication for motor neuron disease?

A

Riluzole - can slow disease progression & extend survival by several MONTHS in ALS

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92
Q

Investigations for Guillian Barre syndrome? (+ their findings)

A
  • Nerve conduction studies(reduced signalthrough nerves)
  • Lumbar punctureforcerebrospinal fluid(showingraised proteinwith a normal cell count and glucose)
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93
Q

Scoring system for GBS?

A

Brighton criteria:
- bilateral weakness of limbs
- decreased tendon reflexes
- absence of alternative diagnosis
- CSF cell count normal
- CSF raised protein
- nerve conduction studies - show reduced conduction

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94
Q

Treatment for GBS?

A
  • IV IG (immunoglobulins) - 1st line
  • Plasmapheresis - 2nd line
  • VTE prophylaxis - to prevent pulmonary embolism (leading cause of death, as muscle weakness causes immobility)
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95
Q

Presentation of GBS?

A

Sympton onset 4 weeks after gastroenteritis
- Symmetrical ascending weakness
- Reduced reflexes
- Peripheral loss of sensation
- Neuropathic pain
- May progress to the cranial nerves and cause facial weakness.
- Autonomic dysfunction can lead to urinary retention, ileus or heart arrhythmias.

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96
Q

Causes of GBS?

A

COMMON - Camplyobacter jejuna
- CMV
- EBV

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97
Q

Antibodies in GBS?

A

Anti-GM1 antibodies = destruction of Schwann cells (PNS)

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98
Q

Diagnostic criteria for neurofibromatosis type 1?

A

CRABBING:
- C–Café-au-lait spots (more than 15mm diameter is significant in adults)
- R–Relative with NF1
- A–Axillary or inguinal freckling
- BB–Bony dysplasia, such asBowing of a long bone or sphenoid wing dysplasia
- I–Iris hamartomas (Lisch nodules) - yellow-brown spots on the iris
- N–Neurofibromas (skin-coloured, raised nodules or papules with a smooth, regular surface)

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99
Q

What tumours are associated with neurofibromatosis type 2?

A

Acoustic neuromas, which are tumours of theauditory nervethat innervates the inner ear.

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100
Q

Causes of peripheral neuropathy?

A

ABCDE (+ Charcot-Marie-Tooth syndrome)

  • A–Alcohol
  • B–B12 deficiency
  • C–Cancer (myeloma) andChronic kidney disease
  • D–Diabetes andDrugs (isoniazid,amiodarone, leflunomideandcisplatin)
  • E–Every vasculitis
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101
Q

Presentation of Charcot-Marie-Tooth disease?

A

Autosomal dominant
Typically at 10 years old, but may be delayed until 40+ years old

  • High foot arches (pes caves)
  • Distal muscle wasting (inverted champagne bottle legs)
  • Loss of ankle dorsiflexion = FOOT DROP!
  • Reduced tendon reflexes
  • Reduced muscle tone
  • Peripheral sensory loss
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102
Q

Physiology of Lambert-Eaton myasthenic syndrome?

A

Autoimmunecondition affecting theNMJ, similar tomyasthenia gravis.
Antibodies againstvoltage-gated calcium channels (in presynaptic membrane of NMJ)

VGCCs destroyed = less Ach released into the synapse, resulting in a weaker signal and reduced muscle contraction.

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103
Q

Disease associated with Lambert-Eaton myasthenic syndrome?

A

Paraneoplastic syndrome occuring alongside small cell lung cancer

(but can also present as a primary AI disorder without SCLC)

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104
Q

Treatment for Lambert-Eaton myasthenic syndrome?

A
  • Amifampridine
  • Pyridostigmine (cholinesterase inhibitor)
  • Immunosuppressants (prednisolone or azathioprine)
  • IV immunoglobulins, or plasmapheresis
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105
Q

Presentation of Lambert-Eaton myasthenic syndrome?

A
  • Proximal muscle weakness difficulty standing from a seat.
  • Autonomic dysfunction - dry mouth, blurred vision, impotence & dizziness
  • Reduced or absent tendon reflexes
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106
Q

How to differentiate Lambert-Eaton + Myasthenia Gravis based on symptoms after a period of muscle contraction?

A

In Lambert-Eaton, signs and symptoms will improve after a period of muscle contraction (i..e improved muscle strength after use, or present tendon reflexes).

Whereas in MG, after muscle usage, the symptoms get progressively worse (fatigued) - symptoms improve with rest!

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107
Q

Which tumours are linked to MG?

A

Strong link withthymomas(thymus gland tumours).
10-20% of patients with MG have a thymoma. 30% of patients with a thymoma develop MG.

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108
Q

Clinical exam to assess muscle fatiguebility in MG?

A
  • ask patient to repeatedly blink to cause ptosis worsening
  • ask to look upwards - worsens diplopia when eyes moved side to side

OR

  • repeatedly abduct arm to the side (up and down) 20 times = leads to unilateral weakness
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109
Q

What is the edrophonium test? (used in MG)

A

Block cholinesterase enzymes that break down Ach = raised levels of Ach = brief relief of muscle weakness

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110
Q

Antibodies present in MG?

A

Ach- receptor antibodies (85%)

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111
Q

Treatments for MG?

A
  • Pyridostigmine/ neostigmine- acetylcholinesterase inhibitors
  • Immunosuppression(prednisolone or azathioprine) suppresses Ab production
  • Thymectomycan improve symptoms, even in patients without a thymoma
  • Rituximab (mAb against B cells) - considered where other treatments fail
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112
Q

Treatment of myasthenic crisis?

A

Acute worsenin gof symptoms, might be triggered by resp. tract infection
=> RESP FAILURE

  • BIPAP / intubation with ventilation
  • IV immunoglobulins or plasmapheresis
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113
Q

Risk factors/associations for subarachnoid haemorrhage?

A
  • Autosomal dominant polycystic kidney disease ⇒ predisposes to berry aneurysms
  • Connective tissue disorders (Marfan or Ehlers-Danlos)
  • Aged 45 to 70
  • Women
  • Black ethnic origin
  • Family history
  • Cocaine use
  • Sickle cell anaemia
  • Neurofibromatosis
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114
Q

CSF findings in subarachnoid haemorrhage?

A
  • raised RBC count in CSF
  • xanthochromia - yellow colour from bilirubin in CSF
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115
Q

Surgical options for extradural and subdural haemorrhages?

A
  • Craniotomy(open surgery by removing a section of the skull)
  • Burr holes (small holes drilled in the skull to drain the blood)
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116
Q

Treatment options for subarachnoid haemorrhage?

A
  • Nimodipine (CCB) - prevents vasospasm (a common complication that causes brain ischaemia)

SURGICAL:
Treat aneurysms with endovascular coiling or neurosurgical clipping.

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117
Q

Presentation of subarachnoid haemorrhage?

A

THUNDERCLAP HEACHAE, SUDDEN ONSET DURING STRENUOUS ACTIVITY

  • Meningism - neck stiffness, photophobia, vomiting)
  • Neurological symptoms(visual changes, dysphasia, focal weakness, seizures and reduced consciousness)
  • Third nerve palsy - oculomotor - compressed by aneurysm on posterior communicating artery
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118
Q

Bell’s palsy?

A

Idiopathic - no apparent cause.
Presents with unilateral lower motor neurone facial nerve palsy.

Most patients fully recover over several weeks, but recovery may take up to 12 months.

  • Forehead affected (unilateral)
  • Ptosis (unilateral)
  • Loss of nasolabial fold (unilateral)
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119
Q

Management of TIA?

A
  • Aspirin 300mg daily (started immediately)
  • Referral for specialist assessment within 24 hours (within 7 days if more than 7 days since the episode)
  • Diffusion-weighted MRI scan
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120
Q

Management of stroke?

A
  • Exclude hypoglycaemia
  • Immediate CT brain to exclude haemorrhage
  • Aspirin 300mg daily for two weeks (started after haemorrhage is excluded with a CT)
  • Admission to a specialist stroke centre:
  • Thrombolysis with alteplase (within 4hrs)
  • Thrombectomy - surgery to remove clot within 24hrs (with confirmed blockage of
    proximal anterior/posterior circulation)
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121
Q

2x investigations for the 2 main underlying causes of stroke or TIA?

A
  • Carotid imaging (e.g., carotid ultrasound, or CT or MRI angiogram)
  • ECG (to look for atrial fibrillation)
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122
Q

Surgical options for confirmed carotid artery stenosis causing stroke/TIA?

A

Considered where there is significant carotid artery stenosis. The options are:

  • Carotid endarterectomy (recommended in the NICE guidelines)
  • Angioplasty and stenting
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123
Q

Secondary prevention of stroke?

A
  • Clopidogrel 75mg OD (alternatively aspirin plus dipyridamole)
  • Atorvastatin 20-80mg (usually delayed at least 48 hours)
  • Blood pressure and diabetes control
  • Addressing modifiable risk factors (e.g., smoking, obesity and exercise)
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124
Q

Brown-seqard ipsilateral vs contralateral losses?

A

=> ipsilateral loss of motor function (corticospinal tract)
=> ipsilateral loss of sensory info about fine touch, vibration, proprioception and pressure (DCML tract)

=> contralateral loss of pain, temp and crude touch (spinothalamic)

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125
Q

Components of GCS score?

A

MOTOR RESPONSE /6
VERBAL RESPONSE /5
EYE OPENING RESPONSE /4

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126
Q

Muscles affected by motor symptoms of carpal tunnel syndrome?

A

Thenar muscles at base of thumb
- Weakness of thumb movements
- Weakness of grip strength
- Difficulty with fine movements involving the thumb
- Wasting of the thenar muscles (muscle atrophy)

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127
Q

Distribution of sensory symptoms of carpal tunnel syndrome?

A

Sensory symptomsin the distribution of the palmar digital cutaneous branchof the median nerve, affecting thepalmar aspectsand fullfingertipsof the:
- Thumb
- Index and middle finger
- The lateral half of ring finger

Sensory symptomsinclude:
- Numbness
- Paraesthesia (pins and needles or tingling)
- Burning sensation
- Pain
(OFTEN WORSE AT NIGHT)

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128
Q

Diagnosis of carpal tunnel? 2x

A
  • Kamath and Stothard carpal tunnel questionnaire (CTQ) - a high score may replace the need for nerve conduction studies to confirm the diagnosis.
  • Nerve conduction studies: a small electrical current is applied by an electrode to the median nerve on one side of the carpal tunnel. Recording electrodes over the median nerve on the other side of the carpal tunnel record the electrical current that reaches them. This demonstrates how well signals are passing through the carpal tunnel along the median nerve.
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129
Q

Improvement of tremor with alcohol - PD or essential tremor?

A

Essential tremor improves with alcohol

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130
Q

Parkinsonism and autonomic dysfunction?

A

Multiple System Atrophy:

Degeneration of the basal ganglia leads to a Parkinson’s presentation. Degeneration in other areas leads toautonomic dysfunction(causing postural hypotension, constipation, abnormal sweating and sexual dysfunction) andcerebellar dysfunction(causingataxia).

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131
Q

Parkinsonism with memory issues?

A

Lewy body dementia

Type of dementia associated with features of Parkinsonism. It causes a progressive cognitive decline. There are associated symptoms ofvisual hallucinations,delusions,REM sleep disordersandfluctuating consciousness.

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132
Q

First line treatment for trigeminal neuralgia?

A

Carbamazapine

TN - intense facial pain that can last for a few seconds to a few hours. The pain is commonly caused by light touch and can occur spontaneously as well.

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133
Q

Treatment for migraine? (2 categories!)

A

Abortive treatment:
- Oral triptan (sumatriptan) + an NSAID or paracetamol
- Anti-emetic (metoclopramide or prochlorperazine)
- Opiatesarenotused to treat migraines and may make the condition worse.

Preventative treatment (if 4-5 attacks a month or interfering with QOL)
- Propranolol OR topiramate (anti-epileptic; teratogenic) or amitriptyline (tricyclic antidepressant)

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134
Q

Treatment for status epilepticus?

A
  • Benzodiazepine (diazepam/midazolam/lorazepam) - repeated after 5-10 minutes if the seizure continues
  • After two doses of benzodiazepine = IV levetiracetam, phenytoin or sodium valproate
  • Third-line options are phenobarbital or general anaesthesia
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135
Q

Cluster headache - treatment + prophylaxis?

A

Treatment: subcutaneous triptans (i.e. sumatriptan)

Prophylaxis: verapamil (CCB) (C for CLUSTER + CCB)

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136
Q

Drugs in AD?

A
  • Acetylcholinesterase inhibitors (rivastigmine + donepezil)
  • MEMANTINE = NMDA receptor agonist
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137
Q

Most likely type of bleed? - head injury with loss of consciousness, followed by lucid period

A

Extradural haemorrhage (LEMON SHAPE)

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138
Q

Most likely type of bleed? - head injury with loss of consciousness, followed by gradual deteroriation

A

Chronic subdural haemorrhage

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139
Q

Investigations + management of DVT?

A
  • Wells score
  • D-dimer
  • Doppler ultrasound
  • CT pulmonary angiogram OR ventilation-perfusion scan - to diagnose PE

= 3 months DOAC (or LMWH in pregnancy)

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140
Q

Investigations for peripheral arterial disease?

A
  • ABPI (ankle-brachial pressure index) <0.9
  • Duplex Doppler ultrasound
  • Buerger’s test - lie patient flat, raise their leg 45º angle for 1 minute. Positive result is if the leg goes pallor and then becomes perfused when restored to normal position. The more severe the ischaemia, the lower the angle is needed to induce pallor. (see photo in SIGNS)
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141
Q

Signs of peripheral arterial disease?

A
  • 6Ps
  • ABPI <0.9
    Leg ulcers
    Xanthomata (yellow cholesterol deposits on the skin)
  • Positive Buerger’s test - if leg goes pale when lifted (in the second part of the test, the leg first goes blue, then turns red)
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142
Q

Treatment options for peripheral arterial disease (intermittment claudication + critical limb ischaemia)

A
  • ‘Graded-exercise therapy’, diet control and smoking cessation.
  • STATINS - atorvastatin** 80mg
  • ANTI-PLATELETS - clopidogrel 75mg OD
  • Naftidrofuryl oxalate (5-HT2 receptor antagonist that acts as a peripheral vasodilator)
  • Endovascular angioplasty with stenting.
  • Endarterectomy– cutting vessel open and removing the atheromatous plaque.
  • Bypass surgery– using a graft to bypass the blockage
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143
Q

Treatment options for peripheral arterial disease? (acute limb-threatening ischaemia)

A

THROMBUS!!
- Surgical emergency, revascularisation is needed within 4-6 hours or else amputation risk is increased.

  • Endovascular thrombolysis - use catheter and insert thrombolysis directly into the clot
  • Endovascular thrombectomy - use catheter to remove thrombus
  • Surgical thrombectomy - cut open vessel to remove thrombus
  • Endartectomy
  • Bypass surgery
  • Amputation
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144
Q

6Ps of acute limb-threatneing ischaemia?

A

Pulselessness
Pallor
Pain
Perishingly cold
Paralysis
Parasthesia

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145
Q

Shockable rhythms?

A

Ventricular fibrillation
Ventricular tachycardia

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146
Q

Non-shockable rhythms?

A

Asystole
Pulseless electrical activity (PEA)

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147
Q

Common causes of AF?

A

SMITH
- Sepsis
- Mitral valve path (sten/regurg)
- Ischaemic HD
- Thyrotoxicosis (hyperthyroidism)
- Hypertension

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148
Q

Causes of secondary hypertension?

A

Secondary HTN = identifiable cause
= ROPED:
- Renal artery stenosis
- Obesity
- Pregnancy
- Endocrine (Conn’s)
- Drugs (alcohol, steroids, oestrogen, NSAIDs)

149
Q

Common side effects of statins?

A

Myalgia (muscle pain)

150
Q

Signs and symptoms of heart failure?

A
  • Ascites
  • Extertional dyspnoea
  • Cough - frothy pink/white sputum
  • Orthopnoea - breathlessness when lying flat, relieved by sitting or standing (ask how many pillows they use)
  • Paroxysmal nocturnal dyspnoea - suddenly waking at night with a severe attack of shortness of breath, cough and wheeze.
  • Peripheral oedema (ankle swelling)
  • Fatigue
  • Tachycardia
  • Displaced apex beat
  • Raised JVP - jugular venous pressure
  • Added heart sounds and murmurs - i.e. 3rd heart sound
  • Hepatomegaly, especially if pulsatile and tender
151
Q

Medical treatment of heart failure?

A

ABAL
AceI
Beta blocker
Aldosterone antagonist (spironolactone/eplerenone)
Loop diuretic (furosemide)

152
Q

Signs of heart failure on chest x-ray?

A

ABCDE
- - Alveolar oedema
- Kerley B lines (interstitial oedema)
- Cardiomegaly
- Dilated prominent upper lobe vessels
- Pleural effusions (blunted costophrenic angle)

153
Q

Which cell line is proliferating in primary myelofibrosis?

A

Haematopoietic stem cells
=> bone marrow fibrosis
=> affects production of blood cells

154
Q

Which cell line is proliferating in polycythaemia vera?

A

Erythroid cells
=> excess RBCs (high Hb)

155
Q

Which cell line is proliferating in essential thrombocythaemia?

A

Megakaryocytes
=> high platelet count

156
Q

Causes of myelofibrosis?

A

Myelofibrosiscan result fromprimary myelofibrosis,polycythaemia veraoressential thrombocythaemia.

157
Q

Blood film finding in myelofibrosis?

A
  • Teardrop-shapedred blood cells )(poikilocytes)
  • Anisocytosis(varying sizes of RBCs)
  • Blasts(immature RBC + WCCS)
158
Q

Bone marrow biopsy findings in myelofibrosis?

A

Bone marrow biopsyis required to confirm the diagnosis.
Bone marrow aspirationmay be “dry” with myelofibrosis, as the bone marrow has turned to scar tissue.

159
Q

Treatment for primary myelofibrosis?

A
  • Chemotherapy (hydroxycarbamide)
  • JAK2 inhibitor (ruxolitinib)
  • Allogeneic stem cell transplantation (risky but potentially curative)
160
Q

Treatment for polycythaemia vera?

A
  • Venesection (excess RBCs)
  • Aspirin (reduce thrombus risk)
  • Chemotherapy (hydroxycarbamide)
161
Q

Treatment for essential thrombocythaemia?

A
  • Anagrelide (platelet-lowering agent)
  • Aspirin (reduce thrombus risk)
  • Chemotherapy (hydroxycarbamide)
162
Q

Presentation of polycythaemia vera?

A
  • Ruddy complexion (red face)
  • Conjunctival plethora (the opposite of conjunctival pallor)
  • Splenomegaly
  • Hypertension
163
Q

Which factor is deficient in Haemophilia A?

A

Factor 8

164
Q

Which factor is deficient in Haemophilia B?

A

Factor 9

165
Q

Inheritance pattern of haemophilia?

A

X-linked recessive

166
Q

Cause of swollen/painful joint in haemophilia?

A

Spontaneous bleeding into joints (haemarthrosis) such as the ankle, knee or elbow can lead to joint damage and deformity.

167
Q

Signs of thalassaemia major?

A
  • Frontal bossing (prominent forehead)
  • Enlarged maxilla (prominent cheekbones)
  • Depressed nasal bridge (flat nose)
  • Protruding upper teeth

Beta thalassaemia major = homozygous 2x deletion genes (no functioning beta-globin genes).
=> severe anaemia
=> bone marrow under so much strain to produce extra RBCs to compensate for the chronic anaemia that it expands enough to increase the risk of fractures and change the patient’s appearance ^

168
Q

Mutations of thalassaemia + chromosome?

A
  • Alpha thalassaemia - chromosome 16 - abnormal a-globin gene
  • Beta thalassaemia - chromosome 11 - abnormal B-globin gene
169
Q

Mutation of sickle cell anaemia + chromosome?

A

Abnormal haemoglobin.
Autosomal recessive; mutation in B-globulin gene on chromosome 11 ⇒ HbS

170
Q

Complications of sickle cell anaemia?

A
  • Vaso-occlusive crisis
  • Priapism - persistent erection
  • Splenic sequestration crisis
  • Aplastic crisis (parvovirus B19 infection - temp. absence of creation of new RBCs - often resolves in 1 week)
  • Acute chest syndrome: vessels supplying lungs clogged with RBCs - hypoxia causes further HbS polymerisation - reduces blood flow further - causes more lung damage
171
Q

2x tests for immune response for TB?

A
  • Mantoux test (tuberculin skin test)
  • Interferon-gamma release assay (IGRA)
    Blood sample is mixed with TB antigens = if they have previously been sensitised, WBCs will release IFG.
172
Q

Investigations for TB?

A
  • Chest x-ray
  • Cultures of deep sputum samples
173
Q

Chest x-ray findings in TB?

A
  • Primary TB -patchy consolidation, pleural effusions and hilar lymphadenopathy.
  • Reactivated TB -patchyornodular consolidation withcavitation (gas-filled spaces), typically in the upper zones.
  • Disseminatedmiliary TB -appearance of millet seedsuniformly distributed across the lung fields.
174
Q

Atypical pneumonia mnemonic?

A

“LegionsofpsittaciMCQs”

  • Legions – Legionella pneumophila.
    Can cause syndrome of inappropriate ADH(SIADH), resulting inhyponatraemia(low sodium).
  • Psittaci – Chlamydia psittaci
    From infected birds (parrots)
  • M – Mycoplasma pneumoniae
  • C – Chlamydophila pneumoniae
    In school age children.
  • Qs – Q fever (coxiella burnetii)
    Body fluids of animals = farmer
175
Q

Signs of cystic fibrosis?

A
  • Low weight or height on growth charts
  • Nasal polyps
  • Finger clubbing
  • Crackles and wheezes on auscultation
  • Abdominal distention
176
Q

Lofgren’s Syndrome?

A

A specific acute clinical presentation of systemic sarcoidosis, consisting of:
- polyarthralgia (joint pain in multiple joints)
- erythema nodosum
- bilateral hilar adenopathy

177
Q

Investigations for sarcoidosis?

A
  • RaisedACE - screening test
  • Raisedcalcium (hypercalcaemia)
  • Chest x-ray + high res CT - shows hilar lymphadenopathy
178
Q

ECG findings for pulmonary embolism?

A

S1 Q3-T3
- S waves in lead I
- Q waves in lead III
- Inverted T waves in lead III

179
Q

What is bronchiectasis?

A

Permanent dilation of the bronchi
Sputum collects (STASIS) here due to the widened tubes

⇒ chronic cough
⇒ continuous sputum production
⇒ recurrent infections

180
Q

Conditions that may lead to bronchiectasis?

A
  • Cystic fibrosis
  • Idiopathic (no apparent cause)
  • Pneumonia
  • Whooping cough (pertussis)
  • Tuberculosis
  • Alpha-1-antitrypsin deficiency
  • Connective tissue disorders (e.g., rheumatoid arthritis)
  • Yellow nail syndrome
181
Q

Chest x-ray signs of bronchiectasis?

A
  • Tram track opacities (parallel markings of a side-view of the dilated airway)
  • Ring shadows (dilated airways seen end-on)
182
Q

Diagnosis of bronchiectasis?

A
  • High resolution CT chest(DIAGNOSTIC)
  • Chest x-ray
  • Sputum culture (for psuedomonas aeruginosa colonisation)
183
Q

Exudative vs transudative pleural effusion?

A
  • Exudative - high protein content (more than 30g/L)
  • Transudative - lower protein content (less than 30g/L)
184
Q

Causes of exudative pleural effusion?

A

Related to inflammation = protein leaking out of tissues

  • Cancer (lung cancer + mesothelioma)
  • Infection (pneumonia + TB)
  • Rheumatoid arthritis
185
Q

Causes of transudative pleural effusion?

A
  • Congestive heart failure
  • Hypoalbuminaemia
  • Hypothyroidism
  • Meigs syndrome
186
Q

What is meigs syndrome?

A

Triad of:
- Benign ovarian tumour
- Pleural effusion
- Ascites

187
Q

Signs of pleural effusion on chest x-ray?

A
  • Bluntingof thecostophrenic angle
  • Fluid in thelung fissures
  • Larger effusions will have ameniscus(curving upwards where it meets the chest wall and mediastinum)
  • Tracheal and mediastinal deviationawayfrom the effusion (in very large effusions)
188
Q

What is empyema?

A

When a pleural effusion becomes infected.

Pleural aspiration will show:
= pus
= low pH
= low glucose (used up by the bacteria)
= high LDH

Treatment:
- Chest drain
- Antibiotics

189
Q

Management of tension pneumothorax?

A

Insert a large bore cannula into the 2nd intercostal space in the midclavicular line.

A chest drain is required for definitive management once the pressure is relieved with a cannula.

190
Q

Presentation of croup?

A
  • Increasedwork of breathing
  • Barking” cough, occurring in clusters of coughing episodes
  • Hoarse voice
  • Stridor (high-pitched inspiratory noise due to upper airway obstruction)
  • Low-gradefever
191
Q

Treatment for otitis media?

A
  • Amoxicillinfor 5-7 days (first-line)
  • Clarithromycin(if penicillin allergic)
  • Erythromycin(in pregnant women allergic to penicillin)
192
Q

Treatment for croup?

A

Dexamethasone

193
Q

Management of epiglottitis?

A

EMERGENCY - skip examinations

  • Ensure airway is secure (prepare to intubate if needed)
  • IV antibiotics (ceftriaxone)
  • Steroids (dexamethasone)
194
Q

Presentation of epiglottitis in a child?

A
  • Tripodposition, sat forward with a hand on each knee
  • Sore throat+stridor
  • Drooling
  • High fever
  • Difficulty or painful swallowing
  • Muffled voice
  • Scared and quiet child
  • Septic and unwell appearance
195
Q

Signs of strep throat?

A

Caused by S.pyogenes (group A)
Strep throat = another type of pharyngitis, can also cause:

  • Difficulty in swallowing
  • Red throat withwhite or grey patches
  • Swollen lymph nodes
  • Fever
  • Loss of appetite
  • Nausea
  • Unusual taste in the mouth
  • General malaise
196
Q

Horner’s syndrome?

A

Ptosis
Miosis (constricted pupil)
Facial anhidrosis (loss of sweating)

197
Q

Alpha-1 antitrypsin deficiency?

A

Autosomal co-dominant genetic conditioncaused by low levels ofalpha-1 antitrypsin:

  • Liver disease (protein retention in liver)
  • Emphysema (lungs disease - damage to alveoli walls)
198
Q

Enzyme affected in alpha-1 antitrypsin deficiency?

A

Alpha-1 antitrypsinoffers protection by inhibiting the action ofneutrophil elastase.

  • Neutrophil elastase breaks down elastic tissue in the lungs => bronchiectasisandemphysema
  • Alpha-1 antitrypsinis produced in theliver. An abnormalmutantversion of the protein is made that gets trapped and builds up inside the liver cells (hepatocytes).
    = inflammation = fibrosis, cirrhosis + hepatocellular carcinoma
199
Q

Hypertonic Saline Stimulation Test?

A

test for diabetes insipidus

  • co-peptin levels (high = confirms nephorgenic DI)
  • give hypertonic saline = stimulates ADH = measures co-peptin again:
    –> still low levels = cranial DI
    –> high levels = primary polydipsia
200
Q

What conditions are associated with Wolfram syndrome?

A

Genetic condition causing diabetes insipidus, diabetes mellitus, optic atrophy and deafness.

201
Q

Renin:aldosterone ratios in primary vs secondary hyperaldosteronism?

A
  • PRIMARY (Conn’s) = adrenal adenoma = high aldosterone, low renin
  • SECONDARY - low BP sensed by kidneys due to renal artery stenosis, HF etc = HIGH RENIN = high aldosterone
202
Q

Causes of primary hyperaldosteronism?

A
  • Adrenal adenoma - secretingaldosterone(Conn’s syndrome)
  • Bilateral adrenal hyperplasia(most common)
  • Familial hyperaldosteronism (rare)
203
Q

Causes of secondary hyperaldosteronism?

A
  • Renal artery stenosis (atherosclerotic narrowing of renal artery)
  • Heart failure
  • Liver cirrhosis and ascites
204
Q

Two types of precocious puberty?

A
  • True (central) - either idiopathic or CNS tumours - treat with GnRH superagonist (suppresses GnRH secretion)
  • Pseudo - tumours drive excess androgens or gonadotropins (not GnRH)
205
Q

Two types of delayed puberty?

A
  • PRIMARY - Hypergonadotrophic hypogonadism
    (lack of oest/test = neg feedback = high GnRH)
  • SECONDARY/TERTIARY - Hypogonadotrophic hypogonadism
    (low GnRH = no gonad stimulation)
206
Q

Causes of hypergonadotrophic hypogonadism?

A
  • Gonad trauma or mumps
  • Kleinfelters (47 XXY)
  • Turners (45 XO)
207
Q

Causes of hypogonadotrophic hypogonadism?

A
  • Damage to hypothalamus/pit gland
  • GH deficiency
  • Constitutional delay in growth and development
  • Kallman syndrome (failure of migration of GnRH neurons) - also associated with anosmia
208
Q

Turner syndrome

A

45 XO
Can cause delayed puberty (hypergonadotrophic hypogonadism)

209
Q

Klinefelter’s syndrome

A

47 XXY
Can cause delayed puberty (hypergonadotrophic hypogonadism)

210
Q

If the CT scan did not confirm subarachnoid haemorrhage, what would you do next to confirm? what would it show?

A

Lumbar puncture
- CSF shows raised RBC count
- CSF shows xanthochromia - yellow colour from bilirubin

211
Q

Features of headache indicating tumour?

A

Worse on waking
Worse on coughing
Postural

212
Q

Investigations for myasthenia gravis?

A

Antibodies (anti-Ach receptor + MuSK + LRP4)

INDUCE MUSCLE FATIGUE (blink to cause ptosis OR abduct arm)

Forced vital capacity (spirometry) - check strength of respiratory muscles

CT/MRI - check for thymoma

Edrophonium test - blocks cholinesterase enzymes that break down Ach = raised levels of Ach = brief relief of muscle weakness

213
Q

Pre-hepatic jaundice?

A

Excessive RBC breakdown = liver cannot conjugate all of the bilirubin
=> excess unconjugated bilirubin

causes: haemolysis (i.e. in sickle cell disease, G6PD deficiency, malaria, autoimmune haemolytic anaemia)

214
Q

Hepatic jaundice?

A

Dysfunction of the hepatic cells - liver cannot conjugate bilirubin
= results in conjugated + unconjugated bilirubin in the blood (’mixed picture’)

Causes: hepatitis, ischaemia, neoplasm, congestive HF

215
Q

Post-renal jaundice?

A

OBSTRUCTIVE - blocks flow of bile
(gallstones, malignancy i.e pancreatic cancer or cholangiocarcinoma, cholangitis, strictures)

Bilirubin not excreted, but has already been conjugated by liver
= conjugated hyperbilirubinaemia

216
Q

Type 4 hypersensitivity?

A

T1DM, Graves, MS
T cell-mediated

217
Q

Type 3 hypersensitivity?

A

RA, SLE, occupational lung disorders
Ag-Ab DEPOSITION

218
Q

Type 2 hypersensitivity?

A

Goodpasture’s
Ag-Ab FORMATION

219
Q

Type 1 hypersensitivity?

A

Anaphylaxis
IgE-mediated

220
Q

Charcot’s neurological triad

A

Seen in MS
- Nstagmus (plaques in nerves of eyes)
- Dysarthria (plques in brainstem)
- Intention tremor (plaques in motor pathways)

221
Q

Pagets disease of bone?

A

Unknown cause
Excessive bone turnover due to increasedosteoclastandosteoblastactivity.

The excessive turnover is not coordinated, leading to patchy areas of high density (sclerosis) and low density (lysis)

222
Q

Pagets disease PRESENTATION?

A

may be asymptomatic

  • Bone pain
  • Bone deformity
  • Fractures
  • Hearing loss
223
Q

Pagets disease - xray findings?

A
  • Bone enlargementanddeformity
  • Osteoporosis circumscripta(well-defined osteolytic lesions)
  • Cotton wool appearanceof theskull
  • V-shaped osteolytic defectsin thelong bones
224
Q

Pagets disease BLOOD FINDING

A

Raised ALP

(normal calcium + phosphate)

225
Q

Management of Pagets disease?

A

Monitoring- check serumalkaline phosphatase(ALP) and review symptoms. Effective treatment should normalise the ALP and eliminate symptoms.

First line: Bisphosphonates

Other measures include:
- Calcitonin - where bisphosphonates are unsuitable
- NSAIDs for bone pain
- Calcium and vitamin D supplementation, if necessary
- Surgery is rarely required to treat fractures, severe deformities and arthritis

226
Q

Cause of osteomalacia?

A

Soft bones
Due to defective bone mineralisation
Caused by VIT D deficiency

227
Q

Treatment for osteomalacia?

A

Colecalciferol(vitamin D₃)

228
Q

Budd-Chiari triad?

A

Abdo Pain, Ascites, Tender Hepatomegaly

An uncommon disorder characterized by obstruction of hepatic venous outflow. The obstruction may be thrombotic or non-thrombotic anywhere along the venous course from the hepatic venules to junction of the inferior vena cava (IVC) to the right atrium.

229
Q

Man has gastroenteritis with bloody diarrhoea. He later develops parasthesia and weakness in his legs, which progresses to his upper limbs. A diagnosis of Guillain-Barre Syndrome (GBS) is suspected and he is started on IV immunoglobulin.

Which of the following is the most likely cause of his gastroenteritis?

A

Campylobacter jejuni
Common cause of GBS

(Shigella is another cause of bloody diarrhoea, but not a cause of GBS)

230
Q

A 45-year-old man presents with abdominal pain, yellowing of the skin and eyes, dark urine, and pale stools. Which of the following is the most likely cause of his jaundice?

A

Gallstones - cause jaundice by obstructing the bile duct, leading to the accumulation of conjugated bilirubin. This leads to pale stools and dark urine.

231
Q

Investigation of hiatus hernia?

A

Barium meal/swallow

232
Q

3 main causes of bowel obstruction?

A

ADHESIONS (scar tissue adhering bowel)
HERNIA
CANCER

233
Q

Management of bowel obstruction?

A

DRIP - IV fluids to rehydrate after their vomiting

SUCK - NG tube to drain stomach contents
(reduces risk of vomiting + aspiration)

234
Q

Chronic mesenteric ischaemia

A

‘Intestinal angina’

Atherosclerosis of mesenteric blood vessels

1) Central colicky abdominal - 30 mins after eating, lasting 1-2 hours

2) Weight loss - due to food avoidance

3) Abdominal bruit (blowing sound caused by turbulent blood flow through blood vessels)

235
Q

Diagnostic investigation for chronic mesenteric ischaemia?

A

CT angiogram

236
Q

Revascularisation procedures for chronic mesenteric ischaemia?

A
  • 1st line - endovascular => percutaneous mesenteric artery stenting

2nd line:
- Endarterectomy (’cleaning out’ blood vessel)
- Re-implantation
- Bypass surgery

237
Q

Cause of acute mesenteric ischaemia?

A

Over 50% mortality

Typically caused by rapid blockage of flow through the superior mesenteric artery

By a THROMBUS, or an embolus (from another site)

238
Q

Diagnostic test for acute mesenteric ischaemia?

A

Contrast CT abdo
=> bowel and blood supply

  • Metabolic acidosis in ABG (raised lactate)
239
Q

What is orthopnoea?

A

Breathlessness when lying flat, relieved by sitting or standing (ask how many pillows they use)

^^symptom of chronic heart failure

240
Q

What is Paroxysmal nocturnal dyspnoea?

A

Describes the experience that patients have of suddenly waking at night with a severe attack of shortness of breath, cough and wheeze.

^^symptom of chronic heart failure

241
Q

Types of kidney stones?

A
  • Calcium (80%) - calcium oxalate & calcium phosphate
  • Uric acid
  • Struvite
  • Cystine
242
Q

Which type of kidney stone is not visible on X-ray?

A

Uric acid stones

243
Q

Which type of kidney stone is associated with bacterial infection?

A

Struvite

244
Q

Which material usually makes up a staghorn calculus?

A

Struvite - form in the shape of renal pelvis during upper UTI

245
Q

Symptoms of kidney/renal stones?

A

Asymptomatic
Renal colic (loin to groin pain)
Haematuria
Reduced urine output
Nause/vomiting

246
Q

Investigations for renal stones?

A
  • Urine dipstick (haematuria)
  • Blood test for kidney function + calcium
  • Non-contrast CT KUB (kidney, ureter, bladder)
  • Ultrasound KUB (in pregnant women + children)
247
Q

Non-surgical management of renal stones?

A
  • NSAIDs
  • Anti-emetics
  • Watchful waiting (0-10mm)
  • Tamsulosin (alpha blocker)
248
Q

Surgical management of renal stones?

A

Surgical interventions required in larger stones (>10mm)

  • Extracorporeal shockwave lithotripsy (under X-ray guidance)
  • Uretroscopy + laser lithotripsy
  • Percutaneous nephrolithotomy (nephroscope inserted in small incision in back)
  • OPEN SURGERY
249
Q

Treatments for prostate cancer?

A
  • Watchful waiting
  • External beam radiotherapy
  • Brachytherapy (radioactive metal seeds = targetted radiotherapy)
  • Hormone therapy - androgen receptor blockers, GnRH agonists (goserelin), GnRH antagonists (degarelix)
  • RADICAL prostatectomy
250
Q

Staging system for testicular cancer?

A

Royal Marsden staging system

  • Stage 1 – isolated to the testicle
  • Stage 2 – spread to the retroperitoneal lymph nodes
  • Stage 3 – spread to the lymph nodes above the diaphragm
  • Stage 4 – metastasised to other organs
251
Q

NICE referral criteria for painless haematuria (2 week wait referral)?

A

Two-week waitreferral for:

  • Aged over 45 withunexplained visible painless haematuria, either without a UTI or persisting after treatment for a UTI
  • Aged over 60 withmicroscopic haematuria (not visible but positive on a urine dipstick)
    PLUS:
  • Dysuria(pain urinating)
    or;
  • Raised white blood cells on FBC
252
Q

Diagnostic investigation for bladder cancer?

A

Flexible cystoscopy(camera through the urethra into the bladder) - rigidorflexible

253
Q

Management of bladder cancer?

A
  • TURBT (transurethral resection of bladder tumour)
  • Intravesical chemotherapy
  • Intravesical BCG - thought to stimulate the immune system
  • Radical cystectomy = remove entire bladder
254
Q

Presentation of renal cell carcinoma?

A

The classic triad of presentation ishaematuria,flank painand apalpable mass.

255
Q

Risk factors for renal cell carcinoma?

A
  • Von Hippel-Lindau Disease
  • Smoking
  • Obesity
  • Hypertension
  • End-stage renal failure
  • Tuberous sclerosis
256
Q

Paraneoplastic features of RCC?

A
  • Polycythaemia– due to excess EPO
  • Hypercalcaemia– due to secretion of a hormone that mimics the action of parathyroid hormone
  • Hypertension– due to various factors, including increased renin secretion, polycythaemia and physical compression
  • Stauffer’s syndrome– abnormal liver function tests (raised ALT, AST, ALP and bilirubin) without liver metastasis
257
Q

Diagnostic investigations in pulmonary embolism?

A

Wells scoreis used when considering pulmonary embolism.
The outcome decides the next step:

  • Unlikely: perform ad-dimer, and if positive, perform aCTPA
  • Likely: CT pulmonary angiogram(CTPA) or alternative imaging (see below)
    • CTPA: chest CT scan with anintravenous contrastthat highlights the pulmonary arteries to demonstrate any blood clots
    • V/Q SPECT scan
    • Planar VQ scan
258
Q

Mode of action of NSAIDs on the GFR?
(why are NSAIDs contraindicated in CKD?)

A

Inhibits prostaglandins = causes vasoconstriction of afferent arteriole

= reduced GFR (hence contraindicated in CKD where GFR is already dangerously low)

259
Q

What part of the kidney does renal cell carcinoma arise from?

A

Proximal renal tubular epithelium

260
Q

Why is renal cell carcinoma associated with polycythaemia?

A

RCC = excess EPO from kidney
= excess RBCs

261
Q

Where does FUROSEMIDE act in the kidney?

A

Thick ascending limb of Loop of Henle

262
Q

Why is sarcoidosis associated with renal stones?

A

Sarcoidoisis = hypercalcaemia
= calcium oxalate renal stones

263
Q

Blood test findings in sarcoidosis?

A
  • RAISED ACE
  • RAISED CALCIUM (hypercalcaemia)
264
Q

Three anatomical locations where ureter narrows, which can cause renal stone obstruction?

A
  • Pelvi-ureteric junction
    (renal pelvis meets ureter)
  • Pelvic brim (overlap with common iliac artery)
  • Vesico-ureteric junction (ureter meets bladder)
265
Q

What type of renal stone is most commonly associated with urease-producing bacteria?

A

Struvite

266
Q

Diagnostic investigatiojn for nephrolithiasis?

A

Non-contrast CT kidney, ureter, bladder

(NCCT-KUB)

267
Q

Lifestyle measures for prevention of renal stone formation in the future?

A

Increase water intake
Reduce sodium diet
Exercise
Reduce oxalate-rich foods
Vit C reduction

268
Q

Side effects of tamsulosin?

A

Alpha-1 blocker in BPH

=> retrograde ejaculation
=> postural hypotension

269
Q

FINASTERIDE - mode of action?

A

Inhibitor of 5-alpha-reductase.

This enzyme changes testosterone to di-hydrotestosterone, which causes the prostate to grow.

Thus, less DHT = decreases prostate size

270
Q

Zones of prostate implicated in BPH vs prostate cancer?

A

BPH = transitional zone

Prostate cancer = peripheral zone

271
Q

Most common cause of nephrotic syndrome in children + in adults?

A

Children = minimal change disease

Adults = focal segmental glomerulosclerosis

272
Q

Diagnostic investigation for nephrotic syndrome?

A

Renal biopsy

273
Q

How can you distinguish between Post-strep glomerulonephritis + IgA nephropathy by their time frames?

A

Post-strep = 1-2 weeks

IgA (Berger’s) = 1-2 days

274
Q

Diagnostic test and value for CF?

A

Sodium chloride sweat test
NaCl >60mmol/L

275
Q

Duration for TB treatment?

A

6 MONTHS:
- 2 months of RIPE
- Further 4 months of RI

276
Q

Causes of Cushing’s syndrome?

A

CAPE

  • Cushing’s disease - pituitary adenoma releasing excess ACTH
  • Adrenal adenoma - adrenal tumour releasing excess cortisol
  • Paraneoplastic syndrome - ectopic ACTH (released from tumour somewhere other than the pituitary gland) ⇒ most common is small cell lung cancer
  • Exogenous steroids - patients taking long-term corticosteroids
277
Q

Metabolic effects of Cushing’s?

A

Hypertension
Cardiac hypertrophy
Type 2 diabetes
Dyslipidaemia (raised cholesterol and triglycerides)
Osteoporosis

278
Q

What is Nelson’s syndrome?

A

Where patients undergo a bilateral adrenalectomy (in cushing’s), an ACTH-producing pituitary tumour may develop due to the lack of cortisol and negative feedback.

Causing:
- Skin pigmentation (high ACTH)
- Bitemporal hemianopia
- Lack of other pit. hormones

279
Q

Short synacthen test?

A

Synthetic ACTH

Give synachten + measure baseline cortisol levels

Measure at 30 + 60 mins

Normally, cortisol will double
=> no increase = primary adrenal insufficiency (Addison’s)

280
Q

How could you measure ACTH levels to distinguish primary + secondary adrenal insufficiency?

A

PRIMARY: ADDISONS = autoimmune destruction of adrenal glands
= high ACTH (due to neg feedback from low cortisol prod.)

SECONDARY: issue with production from pit. gland
= low ACTH (pit gland is not producing ACTH)

281
Q

Renin levels in primary adrenal insufficiency?

A

PRIMARY: ADDISONS = autoimmune destruction of adrenal glands
= low aldosterone
= less Na+/water in = hypotension

==> INCREASE IN RENIN (RAAS system trying to increase BP)

282
Q

Antibodies in Hashimoto vs Graves?

A

HYPO: anti-TPO + anti-Tg

HYPER: anti-TSH receptor

283
Q

Secondary hypothyroidism?

A

Due to pituitary issue or hypothalamus, not THYROID ITESELF
=> NO TSH FROM PIT GLAND

  • pituitary adenomas
  • Sheehan’s syndrome (postpartum haemorrhage causes pituitary gland necrosis)
284
Q

Presentation of polymyositis + dermatomyositis?

A
  • Gradual-onset,symmetrical,proximal muscle weakness, causing difficulties standing from a chair, climbing stairs or lifting overhead.
  • Muscle pain (myalgia), but not always.
  • Dermatomyositis ALSO HAS SKIN FEATURES:
  • Gottron lesions (hands+knees)
  • Heliotrope rash
  • Periorbital oedema
  • Photosensitive erythematous rashon the back, shoulders and neck
285
Q

Diagnosis of polymyositis + dermatomyositis?

A
  • Elevated creatine kinase
  • Autoantibodies
    (ANA + anti-Jo-1 in polymyositis)
  • Electromyography
  • MRI
  • Muscle biopsy
286
Q

Presentation of scleroderma (systemic sclerosis)?

A

LIMITED CUTANEOUS SYSTEMIC SCLEROSIS = CREST
- Calcinosis
- Raynaud’s phenomenon
- Eosophageal dysmotility
- Sclerodactyly
- Telangiectasia
—–

DIFFUSE CUTANEOUS SYSTEMIC SCLEROSIS
= CREST, plus:
- Cardiovascular problems(e.g., hypertension and coronary artery disease)
- Lung problems(pulmonary hypertension and pulmonary fibrosis)
-Kidney problems (glomerulonephritis and scleroderma renal crisis)

287
Q

Autoantibodies for systemic sclerosis / scleroderma?

A
  • ANA
  • Anti-centromere (limited cut SS)
  • Anti-Scl-70 (diffuse cut SS)
288
Q

Diagnosis of systemic sclerosis / scleroderma?

A
  • antibodies (know each)
  • abnormal nailfold
    capillaroscopy (to indicate secondary reynauds)
289
Q

Management of systemic sclerosis / scleroderma?

A

[no standardised treatment)

  • Immunosuppressants + steroids (in diffuse sc ss)
  • Nifedipine - Raynaud’s phenomenon
  • PPI- acid reflux
  • Prokinetic medications - GI symptoms
  • Analgesia (joint pain)
  • Antibioticsfor skin infections
  • Antihypertensives(ACEi) to treat hypertension and scleroderma renal crisis
290
Q

Pathophysiology of Sjogren’s syndrome

A

Autoimmune destructionof theexocrine glands, notably thelacrimalandsalivary glands

=> causing symptoms of dry mouth, eyes and vagina.

[Dry eyes and dry mouth can be calledsiccasymptoms]

More common in women and typically presents in middle age.

291
Q

Diagnosis of Sjogren’s syndrome?

A
  • Anti-Ro
  • Anti-La
  • Schirmer test (<10mm travelled along filter paper)
292
Q

Complications of Sjorgens syndrome

A
  • Eyeproblems -Keratoconjunctivitis sicca andcorneal ulcers
  • Oral problems -dental cavities & candida infections.
  • Vaginalproblems -Candida infectionand sexual dysfunction
293
Q

Presentation of reactive arthritis?

A

CAN’T SEE, CAN’T PEE, OR CLIMB A TREE

  • Bilateral conjunctivitis
  • Anterior uveitis
  • Circinate balanitis
294
Q

Schober’s test?

A

ANKYLOSING SPONDYLITIS

To assess mobility, particularly lumbar spine

  • Patient stands straight
  • Find L5
  • Mark point 10cm above, and 5cm below L5
  • Ask patient to bend forward
  • Measure distance between two points (if its less than 20cm, this indicates restriction of lumbar movement = supports diagnosis)
295
Q

X-ray findings in ankylosing spondylitis?

A
  • Bamboo spine (in late stages)
  • Squaringof the vertebral bodies
  • Subchondral sclerosisanderosions
  • Ossificationof the ligaments, discs and joints (structures start turning into bone)
  • Fusionof thefacet,sacroiliacandcostovertebraljoints
296
Q

Arthritis mutilans

A

Most severe form of psoriatic arthritis

  • Osteolysis of bones
    = shortening of fingers
    = skin folds
    = TELESCOPING

‘PENCIL-IN-CUP ON XRAY’

297
Q

Most common cause of osteomyelitis in:
- normal
- IVDU
- post-op

A

Normal - S.aureus

IVDU - pseudomonas aeruginosa

Post-op joint replacement - S.epidermidis

Sickle cell anaemia - Salmonella

298
Q

Management of osteomyelitis?

A
  • 6 weeks flucloxacillin if acute, 3 months if chronic
  • Surgical debridement of bone
299
Q

Antibodies in anti-phospholipid syndrome?

A
  • Lupus anticoagulant
  • Anticardiolipin antibody

→ two or more occasions at least 12 weeks apart can confirm the diagnosis of APS

These antibodies bind to the phospholipids on the surface of cells, causing inflammation and increasing the risk of thrombosis.

300
Q

Main features of anti-phospholipid syndrome?

A

CLOT

C - clots (VTE)
L - livedo reticularis (mottled lower limbs)
O - obstetric loss
T - thrombocytopenia

301
Q

Autoantibodies in SLE?

A

ANA
Anti-dsDNA

302
Q

Man started on allopurinol (xanthine oxidase inhibitor) weeks after initial gout attack. What do we need to also give acutely?

A

NSAIDs

Allopurinol can acutely raise the level of urate (and precipitate or worsen a flare of gout) before lowering the levels of gout. Therefore covering with an NSAID is important for reducing the risk of another flair while allopurinol therapy is initiated

303
Q

Live vaccines?

A

MMR BOY (Measles, Mumps, Rubella; BCG; Oral Polio; Yellow Fever)

304
Q

Which vessel is ischaemic stroke?
- Jumbled words, RHS visual issues, RHS facial droop and hemiplegia

A

Left middle cerebral artery

(look at stick man diagram on Notion stroke page)

305
Q

A 27 year old woman presents to hospital with a 1 hour history of a severe, sudden onset headache. She informs you that it felt like someone had hit the back of her head with a baseball bat. She says it is the worse headache she has ever had. She is also complaining of photophobia but has no infective symptoms. She has no significant past medical history.

CT head is unrevealing.

Which of the following is the next best investigation to confirm the diagnosis?

A

Lumbar puncture 12 hours after symptom onset

  • CSF shows xanthochromia - yellow colour from bilirubin
  • CSF shows raised RBC count
306
Q

Causes of infective endocarditis?

A

General pop + poor dental hygiene - S.viridans
IVDU - S.aureus
Prosthetic valves - S.epidermidis

307
Q

Signs of HF on chest xray?

A

ABCDE
Alveolar oedema
Kerley B lines
Cardiomegaly
Dilated upper lobe vesssels
Effusion (pleural)

308
Q

ECG changes in STEMI vs NSTEMI?

A

STEMI:
1) ST-segment elevation
2) New left bundle branch block

NSTEMI
1) ST segment depression
2) T wave inversion

309
Q

When is troponin raised?

A

Used to diagnose NSTEMI (not required in STEMI, as this is based on ECG + clinical findings)

Non-specific - also raised in:
- Chronic kidney disease
- Sepsis
- Myocarditis
- Aortic dissection
- Pulmonary embolism

310
Q

Which joints are spared at onset of RA?

A

DIP distal interphalangeal joints

311
Q

Which joints are spared at onset of RA?

A

DIP distal interphalangeal joints

312
Q

COPD severity scale (FEV1)

A

Graded using theforced expiratory volumein 1 second(FEV1):

  • Stage 1 (mild): FEV1 more than 80% of predicted
  • Stage 2 (moderate): FEV1 50-79% of predicted
  • Stage 3 (severe): FEV1 30-49% of predicted
  • Stage 4 (very severe): FEV1 less than 30% of predicted
313
Q

Name 3 risk factors for CKD development.

A

T2DM
Hypertension
Glomerulonephritis
NSAID use
PKD - polycystic kidney disease

314
Q

Suggest 4 complications of CKD.

A

Anaemia
Osteoporosis
CVD
Encephalopathy/neuropathy

315
Q

Name 4 investigations you could perform in a patient with CKD.

A

FBC
U&Es
Renal ultrasound scan
Urine dip
eGFR
A:Cr ratio (albumin:creatinine ratio)

316
Q

Courvoisier sign?

A

Enlarged gallbladder + painless jaundice
(sign of pancreatic cancer)

Courvoisier’s law states that the presence of a non-tender ENLARGED/PALPABLE gallbladder means that jaundice isunlikely to be due to gallstones = therefore it is a red flag for pancreatic cancer

317
Q

Reynold’s pentad?

A

5 factors:
Charcot’s triad + hypotension/shock + confusion

(Charcot’s triad is RUQ pain, fever + jaundice)

318
Q

Drug treatments for idiopathic pulmonary fibrosis?

A

Anti-fibrotics (nintedanib or pirfenidone).

319
Q

Common associations of sarcoidosis?

A
  • LUNGS: pulmonary fibrosis, mediastinal lymphadenopathy
  • SKIN: erythema nodosum
  • EYES: uveitis, conjunctivitis, optic neuritis

KIDNEY: renal stones (due to hypercalcaemia)

CNS: encephalopathy

BONES: arthralgia, arthritis

320
Q

Dull vs stony dull percussion?

A

Stony dull percussion - pleural effusion.

Dull percussion - pneumonia

321
Q

Investigations in suspected pulmonary fibrosis?

A
  • DIAGNOSTIC =>
    HRCT: high-resolution CT thorax (show honeycombing)
  • Spirometry (normal or restrictive >70% FEV1:FVC ratio)
322
Q

Give 2 common organisms that can cause an infective exacerbation of COPD

A

most common organism = haemophilus influenzae.

Others = strep pneumoniae, Moraxella catarrhalis

323
Q

Which spirometry results indicate an obstructive respiratory disease?

A

FEV1 <0.8 predicted (severity scale - GOLD)

FEV1/FVC <0.7

324
Q

Chest xray findings in COPD?

A

Hyperinflation - enlarged lungs.

Air pockets (bullae)

Flattened diaphragm

325
Q

Chest xray findings in TB?

A

Bilateral hilar lymphadenopathy

Ghon focus (primary lesion)

Effusions

326
Q

Risk factors for TB?

A

Immunosuppression (HIV)
Ethnicity
IVDU
Homeless/overcrowded housing
Close contact with infected person

327
Q

Acute asthma attack management?

A

OSHITME

O2, SABA, Hydrocortisone, Ipratropium, Theophylline, Mg sulfate, Escalate

328
Q

Give 4 triggers for allergic asthma

A

Cold temp, exercise, dust, NSAIDs, beta-blockers, infection, stress, allergens

329
Q

Name 4 signs of poorly controlled asthma in the history

A

Nocturnal cough, multiple exacerbations, wheeze, recessions, hyperinflated chest

330
Q

List three complications that can arise as a result of chronic liver disease

A

Ascites

Portal hypertension = GI bleeding /varices /variceal bleed

Hepatic Encephalopathy

Spontaneous bacterial peritonitis
Hepatocellular carcinoma Malnutrition
Splenomegaly, thrombocytopenia, Hepato Renal Syndrome, Hepatic Failure, Infection, Pulmonary Complication, Porto pulmonary hypertension, Hepato-pulmonary syndrome (HPS), Hepatic hydrothorax, coagulation defects, Osteoporosis

331
Q

Name 1 blood marker that may be used to monitor progression of pancreatic cancer?

A

Ca 19-9

(raised in cholangiocarcinoma, pancreatic cancer + gastric cancer)

332
Q

Diagnostic investigations for ACHALASIA?

A
  • Barium swallow ⇒ bird’s beak sign
  • Manometry - measures muscle pressure
  • OGD (oesophago-gastro-duodenoscopy) to exclude oesophageal cancer
333
Q

Treatment for ACHALASIA?

A

Surgery is curative

  • Balloon dilation (using endoscope)
  • Laparoscopic (keyhole) cardiomyotomy / Heller’s procedure - cut the muscle fibres (lower oesophageal sphincter)⇒ causes iatrogenic GORD - so they can also perform Nissen’s fundoplication at the same time.
334
Q

Extraintestinal signs of IBD?

A

APIESAC
- Aphthous ulcers (mouth)
- Pyoderma gangrenosum(rapidly enlarging, painful skin ulcers)
- Iritis(episcleritis, scleritis and anterior uveitis)
- Erythema nodosum(red nodules on shins)
- Sclerosing cholangitis (PSC - particularly with ulcerative colitis)
- **Arthritis (enteropathic)
- Clubbing of fingers

  • EYE (episcleritis, anterior uveitis)
  • Enteropathic arthritis (spondylarthropathy)
  • Erythema nodosum
  • Pyoderma gangrenous
335
Q

Signs of appendicitis?

A

Rovsing’s sign (palpation of theleft iliac fossacauses pain in theRIF)

Rebound tendernessin the RIF (increased pain whensuddenlyreleasingthe pressure of deep palpation)

Central abdominal pain = moves to right iliac fossa in first 24 hours

Guarding on abdominal palpation (voluntary contraction of the abdominal wall musculature to avoid pain)

Tenderness at McBurney’s point

336
Q

Clinical signs of peritonitis?

A
  • Rebound tendernessin the RIF (increased pain whensuddenlyreleasingthe pressure of deep palpation)
  • Percussion tenderness(pain and tenderness when percussing the abdomen)

Rebound tendernessandpercussion tendernesssuggestperitonitis, potentially indicating aruptured appendix.

337
Q

Causes of peritonitis?

A
  • Appendicitis = ruptured appendix
  • Stomach or duodenal ulcer perforation
  • Cirrhosis = spont. bacterial peritonitis
  • Pancreatitis or cholecystitis (tend to be localised)
  • Perforated diverticulum
  • Peritoneal dialysis - external contamination
  • In females - pelvic inflammatory disease
338
Q

Risk factors for colorectal cancer?

A
  • Family history of bowel cancer
  • IBD
  • Diet (high in red and processed meat and low in fibre)
  • Obesity and sedentary lifestyle
  • Smoking
  • Alcohol

Autosomal dominant:
- Familial adenomatous polyposis(FAP)
- HNPCC / hereditary nonpolyposis colorectal cancer (Lynch syndrome)

339
Q

Antibiotics that inhibit protein synthesis? (target ribosome)

A

Macrolides (clarithromycin + erythromycin)
Chloramphenicol
=> inhibit 50S subunit

Tetracyclines (doxycycline)
Aminoglycosides (gentamicin)
=> inhibit 30S subunit

340
Q

Antibiotics that inhibit cell wall synthesis?

A

Penicillins
Cephalosporins
Carbapenems
Glycopeptides (vancomycin + teicoplanin)

341
Q

Antibiotics that inhibit folic acid metabolism?

A

Sulfamethoxazole
Trimethoprim

342
Q

Antibiotics that inhibit nucleic acid metabolism?

A

Metronidazole
Ciprofloxacin
Trimethoprim

343
Q

Extraarticular manifestations in in ankylosing spondylitis?

A
  • A–Anterior uveitis
  • A–Aortic regurgitation
  • A–Atrioventricular block (heart block)
  • A–Apical lung fibrosis (fibrosis of theupper lobesof the lungs)
  • A–Anaemia of chronic disease
344
Q

Chromosomes that translocate - Philadelphia chromosome?

A

t(9;22)

345
Q

Peak flow values for each asthma severity classification?

A

MODERATE:  50-75% best or predicted

ACUTE SEVERE: 33-50% best or predicted

LIFE-THREATENING: < 33% best or predicted

346
Q

Investigation of upper GI bleed?

A

Oesophago-gastro-duodenoscopy (OGD) (endoscopy) is required to diagnose and treat the source of the bleeding

347
Q

definition of a granuloma?

A

an aggregation of epitheloid histocytes

348
Q

Management of nephrotic syndrome?

A
  • High dose steroids (prednisolone)
    Given for 4 weeks, then weaned over further 8 weeks
  • Low salt diet
  • Diuretics - for oedema
349
Q

Complications of nephrotic syndrome?

A
  • Hypovolaemia - causing low BP
  • Thrombosis - due to loss of albumin which normally prevents clotting, also liver responds to low albumin by producing pro-thrombotic proteins
  • Infection
  • Acute or chronic renal failure
  • Relapse
350
Q

Management of GORD

A
  • Reviewing medications(stop NSAIDs)
  • Proton pump inhibitors(omeprazole and lansoprazole)
  • Antacids(Gaviscon + Rennie) – short term only
  • Histamine H2-receptor antagonists(famotidine)
  • Surgery - laproscopic fundoplication - tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter.
351
Q

Components of non-invasive liver screen?

A

liver function tests - including gamma GT and total protein
ethanol
coagulation tests, including INR and APTT
hepatitis serology - for A, B, and C
viral screen, for CMV, EBV etc
ferritin and total iron binding capacity
immunoglobulins and protein electrophoresis
autoantibody screen
alpha-feto protein
alpha 1 antitrypsin
serum copper, ceruloplasmin, 24 hour copper
Anti-mitochondrial antibodies
Anti-nuclear antibodies

352
Q

three cardinal signs of heart failure

A

shortness of breath, fatigue and ankle oedema

353
Q

Biopsy histology findings in coeliac disease?

A

in small intestine - mainly jejunum

  • Raised intra-epithelial lymphocytes
  • Villous atrophy
  • Crypt hyperplasia
354
Q

adolescent with a sore throat, who develops an itchy rash after taking amoxicillin?

A

Infectious mononucleosis (glandular fever) causes an intensely itchy maculopapular rash in response to amoxicillin or cefalosporins.(given these for wrongly presumed tonsilittis)

355
Q

Risk factors for osteoporosis?

A

SHATTERED FAMILY
Steroid use
Hyperthyroidism/hyperPTH
Alcohol + smoking
Thin (BMI<22)
Testosterone (LOW)
Early menopause
Renal/liver failure
Erosive bone disease (RA)
Diabetes
FAMILY HISTORY

356
Q

First line med for osteoporosis?

A

Bisphosphonates

(alendronate, risedronate, zoledronic acid)

357
Q

Instructions for taking bisphosphonates in osteoporosis?
+ reason for this (i.e. side effects)

A

first thing in the morning - empty stomach with glass of water - sit upright for 30 mins

  • reflux
  • oesophageal erosions

other SEs:
- atypical fractures
- jaw osteonecrosis

358
Q

Components of Glasgow-Blatchford score?

A

A score above 0 indicates a high risk for an upper GI bleed.

  • Haemoglobin (falls in upper GI bleeding)
  • Urea (rises in upper GI bleeding)
  • Systolic blood pressure
  • Heart rate
  • Melaena(black, tarry stools)
  • Syncope(loss of consciousness)
  • Liver disease
  • Heart failure
359
Q

Which benzodiazepine may be used to manage the effects of alcohol withdrawal?

A

Chlordiazepoxide

360
Q

Extradural vs subdural haematoma SHAPE?

A

Subdural - banana (S saucy)
Extradural - lemon (extra zingy)

361
Q

Typical x-ray changes seen in patients with myeloma

A

Well-defined lytic lesions (described as looking “punched-out”)
Diffuse osteopenia
Abnormal fractures

Raindrop skull/pepper pot skull - refers to multiple lytic lesions seen in the skull

362
Q

Features of decompensated liver disease?

A

A – Ascites
H – Hepatic encephalopathy
O – Oesophageal varices bleeding
Y – Yellow (jaundice)

363
Q

Monitoring for complications in liver cirrhosis?

A
  • MELD score every 6 months
  • Ultrasound + alpha-fetoprotein every 6 months for hepatocellular carcinoma
  • Endoscopy every 3 years for oesophageal varices
364
Q

Complications of liver cirrhosis?

A
  • Malnutrition+muscle wasting
  • Portal hypertension,oesophageal varices(+bleeding varices)
  • Ascites+spontaneous bacterial peritonitis
  • Hepatorenal syndrome
  • Hepatic encephalopathy
  • Hepatocellular carcinoma
365
Q

Management options for ascites in liver cirrhosis?

A
  • Low sodium diet
  • Aldosterone antagonists(spironolactone)
  • Paracentesis(ascitic tap or ascitic drain)
  • Prophylactic antibiotics(ciprofloxacin/norfloxacin) when there is <15 g/litre of protein in the ascitic fluid
  • Transjugular intrahepatic portosystemic shunt(TIPS) - inrefractory ascites
  • Liver transplantation - inrefractory ascites
366
Q

Examination findings in liver cirrhosis?

A
  • Cachexia(wasting of the body and muscles)
  • Jaundice-raised bilirubin
  • Hepatomegaly (then small nodular liveras it becomes more cirrhotic)
  • Splenomegalydue toportal hypertension
  • Spider naevi(telangiectasia with a central arteriole and small vessels radiating away)
  • Palmar erythemacaused by elevated oestrogen levels
  • Gynaecomastiaandtesticular atrophyin males due to endocrine dysfunction
  • Bruisingdue to abnormal clotting
  • Excoriations(scratches on the skin due to itching)
  • Ascites
  • Caput medusae(distended paraumbilical veins due toportal hypertension)
  • Leukonychia(white fingernails) associated withhypoalbuminaemia
  • Asterixis(“flapping tremor”) indecompensated liver disease
367
Q

What do we co-prescribe with RIPE drugs for TB? (for side effects)

A

Pyridoxine
- Isoniazid - causes peripheral neuropathy, so co-prescribe pyridoxine (vitamin B6) to prevent this.

368
Q

Risk factors for psuedogout? (chondrocalcinosis)

A

-Older age
- Haemochromatosis (iron deposits in joints)
- Hyperparathyroidism (=high calcium)
- Hypophosphatasia
- Hypomagnesaemia
- Hypothyroidism
- Acromegaly

Phase 2a (5 decks)

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