Wednesday [26/4/23]

Question 1

what should all patients recieve in angina pectoris? [2]

Answer 1

statin and aspirin

Question 2

what to abort attacks angina? [1]

Answer 2

GTN spray

Question 3

which medication first-line Mx angina pectoris? [2]

Answer 3

BB or CCB [verapamil or diltiazem]

Question 4

what should not be Rx with verapamil? [1]

Answer 4

beta blocker, as risk heart block

Question 5

what should you do before starting other Tx angina? [2]

Answer 5

so first maximum dose of monotherapy, then add in another drug

Question 6

dosing with nitrates [2]

Answer 6

often patients will develop tolerance, so NICE advises asymmetric dosing

Question 7

Which one of the following cardiac conditions is most associated with a louder murmur following the Valsalva manoeuvre?

Answer 7

HOCM

Question 8

echo findings in HOCM

Answer 8

mitral regurgitation (MR)
systolic anterior motion (SAM) of the anterior mitral valve leaflet
asymmetric hypertrophy (ASH)

Question 9

strategy for who should be started on statins? [2]

Answer 9

A systematic strategy should be used to identify people aged over 40 years who are likely to be at high risk of cardiovascular disease (CVD), defined as a 10-year risk of 10% or greater. QRISK2.

Question 10

primary prevention statin for which groups? [3]

Answer 10

20mg atorvastatin: QRISK above 10%, T1DM, or eGFR less than 60

Question 11

secondary prevention statins? [1]

Answer 11

known IHD OR CVD OR PAD

Question 12

what is PBC? [2]

Answer 12

Primary biliary cholangitis (previously referred to as primary biliary cirrhosis) is a chronic liver disorder typically seen in middle-aged females (female:male ratio of 9:1). The aetiology is not fully understood although it is thought to be an autoimmune condition. Interlobular bile ducts become damaged by a chronic inflammatory process causing progressive cholestasis which may eventually progress to cirrhosis. The classic presentation is itching in a middle-aged woman

Question 13

first line medication PBC? [1]

Answer 13

Ursodeoxycholic acid is the first-line medication for primary biliary cholangitis

Question 14

which antibodies are seen in PBC? [1]

Answer 14

Primary biliary cholangitis (previously referred to as primary biliary cirrhosis) is a chronic liver disorder typically seen in middle-aged females and is usually associated with other autoimmune diseases such as Sjogren’s syndrome. Anti-mitochondrial antibodies (AMA) M2 subtype are present in 98% of patients and are highly specific.

Question 15

clinical features of PBC [5]

Answer 15

early: may be asymptomatic (e.g. raised ALP on routine LFTs) or fatigue, pruritus
cholestatic jaundice
hyperpigmentation, especially over pressure points
around 10% of patients have right upper quadrant pain
xanthelasmas, xanthomata
also: clubbing, hepatosplenomegaly
late: may progress to liver failure

Question 16

Mx of PBC [2]

Answer 16

first-line: ursodeoxycholic acid
slows disease progression and improves symptoms
pruritus: cholestyramine
fat-soluble vitamin supplementation
liver transplantation
e.g. if bilirubin > 100 (PBC is a major indication)
recurrence in graft can occur but is not usually a problem

Question 17

Cx of PBC [3]

Answer 17

cirrhosis → portal hypertension → ascites, variceal haemorrhage
osteomalacia and osteoporosis
significantly increased risk of hepatocellular carcinoma (20-fold increased risk)

Question 18

Cause of low magnesium

Answer 18

drugs
diuretics
proton pump inhibitors
total parenteral nutrition
diarrhoea
may occur with acute or chronic diarrhoea
alcohol
hypokalaemia
hypercalcaemia
e.g. secondary to hyperparathyroidism
calcium and magnesium functionally compete for transport in the thick ascending limb of the loop of Henle
metabolic disorders
Gitleman’s and Bartter’s

Question 19

features of low magnesium

Answer 19

paraesthesia
tetany
seizures
arrhythmias
decreased PTH secretion → hypocalcaemia
ECG features similar to those of hypokalaemia
exacerbates digoxin toxicity

Question 20

Tx of low magnesium

Answer 20

<0.4 mmol/L or tetany, arrhythmias, or seizures
intravenous magnesium replacement is commonly given.
an example regime would be 40 mmol of magnesium sulphate over 24 hours

> 0.4 mmol/l
oral magnesium salts (10-20 mmol orally per day in divided doses)
diarrhoea can occur with oral magnesium salts

Question 21

where do 5-HT3 antagonists act? [3]

Answer 21

5-HT3 antagonists are antiemetics used mainly in the management of chemotherapy-related nausea. They mainly act in the chemoreceptor trigger zone area of the medulla oblongata.

Examples
ondansetron
palonosetron
second-generation 5-HT3 antagonist
main advantage is reduced effect on the QT interval

Question 22

retroperitoneal organs

Answer 22

S: supearenal (adrenal) gland
A: aorta
D: duodenum
P: pancreas
U: ureter
C: colon
K: kidneys
E: Esophagus
R: rectum

Question 23

which organ in direct contact with left kidney [2]

Answer 23

pancreas

Question 24

causes of COPD

Answer 24

Smoking!

Alpha-1 antitrypsin deficiency

Other causes
cadmium (used in smelting)
coal
cotton
cement
grain

Question 25

what should be given pregnancy? [1]

Answer 25

Which one of the following interventions should be offered to reduce the risk of developing pre-eclampsia again?

Question 26

painful third nerve palsy which artery? [1]

Answer 26

Painful third nerve palsy = posterior communicating artery aneurysm

Question 27

features of third nerve palsy [2]

Answer 27

eye is deviated ‘down and out’
ptosis
pupil may be dilated (sometimes called a ‘surgical’ third nerve palsy)

Question 28

Ix for PSC

Answer 28

endoscopic retrograde cholangiopancreatography (ERCP) or magnetic resonance cholangiopancreatography (MRCP) are the standard diagnostic investigations, showing multiple biliary strictures giving a ‘beaded’ appearance
p-ANCA may be positive
there is a limited role for liver biopsy, which may show fibrous, obliterative cholangitis often described as ‘onion skin’

Question 29

What is PSC, associations and features [3]

Answer 29

Primary sclerosing cholangitis is a biliary disease of unknown aetiology characterised by inflammation and fibrosis of intra and extra-hepatic bile ducts.

Associations
ulcerative colitis: 4% of patients with UC have PSC, 80% of patients with PSC have UC
Crohn’s (much less common association than UC)
HIV

Features
cholestasis
jaundice, pruritus
raised bilirubin + ALP
right upper quadrant pain
fatigue

Question 30

XR findings of AS

Answer 30

Ankylosing spondylitis - x-ray findings: subchondral erosions, sclerosis
and squaring of lumbar vertebrae

Question 31

SE of RIPE medications

Answer 31

Rifampicin
mechanism of action: inhibits bacterial DNA dependent RNA polymerase preventing transcription of DNA into mRNA
potent liver enzyme inducer
hepatitis, orange secretions
flu-like symptoms

Isoniazid
mechanism of action: inhibits mycolic acid synthesis
peripheral neuropathy: prevent with pyridoxine (Vitamin B6)
hepatitis, agranulocytosis
liver enzyme inhibitor

Pyrazinamide
mechanism of action: converted by pyrazinamidase into pyrazinoic acid which in turn inhibits fatty acid synthase (FAS) I
hyperuricaemia causing gout
arthralgia, myalgia
hepatitis

Ethambutol
mechanism of action: inhibits the enzyme arabinosyl transferase which polymerizes arabinose into arabinan
optic neuritis: check visual acuity before and during treatment
dose needs adjusting in patients with renal impairment

Question 32

Long QT syndrome causes

Answer 32

Congenital Drugs* Other
Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel)
Romano-Ward syndrome (no deafness)
amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram)
methadone
chloroquine
terfenadine**
erythromycin
haloperidol
ondanestron
electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia
acute myocardial infarction
myocarditis
hypothermia
subarachnoid haemorrhage

Question 33

hand changes psoriatic arthritis

Answer 33

Inflammatory arthritis involving DIP swelling and dactylitis points to a diagnosis of psoriatic arthritis

Question 34

features of SLE [10]

Answer 34

Serositis: pleurisy or pericarditis
Oral ulcers
Arthritis
Photosensitivity

Blood: anaemia, leukopenia, lymphopenia and thrombocytopenia
Renal disorder: lupus nephritis - minimal mesangial, mesangial proliferative, focal, diffuse, membranous and advanced sclerosis
Antinuclear antibody
Immunology: anti-Smith, anti-ds DNA and antiphospholipid antibody
Neurologic disorder: seizures or psychosis

Malar rash
Discoid rash

Question 35

types of IG

Answer 35

Type Frequency Shape Notes
IgG 75% Monomer * Enhance phagocytosis of bacteria and viruses
* Fixes complement and passes to the fetal circulation
* Most abundant isotype in blood serum
IgA 15% Monomer/ dimer * IgA is the predominant immunoglobulin found in breast milk. It is also found in the secretions of digestive, respiratory and urogenital tracts and systems
* Provides localized protection on mucous membranes
* Most commonly produced immunoglobulin in the body (but blood serum concentrations lower than IgG
.)
* Transported across the interior of the cell via transcytosis
IgM 10% Pentamer * First immunoglobulins to be secreted in response to an infection
* Fixes complement but does not pass to the fetal circulation
* Anti-A, B blood antibodies (note how they cannot pass to the fetal circulation, which could of course result in haemolysis)
Pentamer when secreted
IgD 1% Monomer * Role in immune system largely unknown
* Involved in activation of B cells
IgE 0.1% Monomer * Mediates type 1 hypersensitivity reactions
* Synthesised by plasma cells
* Binds to Fc receptors found on the surface of mast cells and basophils
* Provides immunity to parasites such as helminths
* Least abundant isotype in blood serum

Question 36

How does HACE present? [2]

Answer 36

A minority of people above 4,000m go onto develop high altitude pulmonary oedema (HAPE) or high altitude cerebral oedema (HACE), potentially fatal conditions
HAPE presents with classical pulmonary oedema features
HACE presents with headache, ataxia, papilloedema

Question 37

preventino of HACE

Answer 37

Prevention and treatment of AMS
the risk of AMS may actually be positively correlated to physical fitness
gain altitude at no more than 500 m per day
acetazolamide (a carbonic anhydrase inhibitor) is widely used to prevent AMS and has a supporting evidence base
it causes a primary metabolic acidosis and compensatory respiratory alkalosis which increases respiratory rate and improves oxygenation
treatment: descent

Question 38

Mx of HACE [2]

Answer 38

descent, dexamethasone

Question 39

examples of quinolones [2]

Answer 39

ciprofloxacin, levofloxacin

Question 40

risk of quinolones

Answer 40

lower seizure threshold in patients with epilepsy
tendon damage (including rupture) - the risk is increased in patients also taking steroids
cartilage damage has been demonstrated in animal models and for this reason quinolones are generally avoided (but not necessarily contraindicated) in children
lengthens QT interval

Question 41

CI for quinolones

Answer 41

women pregnant or breastfeeding

Question 42

gram positive cocci

Answer 42

Therefore, only a small list of Gram-positive rods (bacilli) need to be memorised to categorise all bacteria - mnemonic = ABCD L
Actinomyces
Bacillus anthracis (anthrax)
Clostridium
Diphtheria: Corynebacterium diphtheriae
Listeria monocytogenes

Remaining organisms are Gram-negative rods, e.g.:
Escherichia coli
Haemophilus influenzae
Pseudomonas aeruginosa
Salmonella sp.
Shigella sp.
Campylobacter jejuni

Question 43

gram negative cocci

Answer 43

Therefore, only a small list of Gram-positive rods (bacilli) need to be memorised to categorise all bacteria - mnemonic = ABCD L
Actinomyces
Bacillus anthracis (anthrax)
Clostridium
Diphtheria: Corynebacterium diphtheriae
Listeria monocytogenes

Remaining organisms are Gram-negative rods, e.g.:
Escherichia coli
Haemophilus influenzae
Pseudomonas aeruginosa
Salmonella sp.
Shigella sp.
Campylobacter jejuni

Question 44

types of AF

Answer 44

A patient with persistent AF is one who experiences AF at all times
This is defined by the AHA/ACC/HRS guidelines (2014) as ‘continuous AF that is sustained for more than 7 days’
These guidelines also note that some patients in this group can be described as having permanent AF, where a return to sinus rhythm is no longer part of their treatment plan
A patient with paroxysmal AF only experiences AF at certain times. At all other times their heart contracts in sinus rhythm
This is defined by the AHA/ACC/HRS guidelines (2014) as ‘AF that terminates spontaneously within 7 days of onset’
Most patients in this group have multiple short episodes of AF which may or may not have an obvious trigger
Paroxysmal AF can progress to persistent AF over the course of many years. The AHA/ACC/HRS guidelines (2014) note that episodes of paroxysmal AF occur more often and for a longer duration as the condition progresses

Question 45

signs of haemodynamic compromise in AF

Answer 45

Heart Rate >150 bpm
Blood Pressure <90 mmHg
Syncope or severe dizziness
Shortness of breath
Chest Pain

Question 46

when are echos indicated for AF

Answer 46

Indication: 2014 NICE guidelines recommend that echocardiograms should be used in patients where the investigation may aid in acute or long term management or in whom an underlying cardiac risk factor is suspected. In contrast the 2014 AHA/ACC/HRS guidelines recommend echocardiograms are used in all patients with a diagnosis of AF, but this may not be feasible in many clinical contexts

Question 47

rate control

Answer 47

beta-blockers
Non-Dihydropyridine Calcium Channel Blockers such as verapamil and diltiazem
NICE (2014) recommend that physicians should decide between these two drugs based on patient factors, such as co-morbidities
Digoxin can be used, but NICE (2014) do not recommended its use outside of sedentary patients with non-paroxysmal AF
It is important to note that, as mentioned in the AHA/ACC/HRS guidelines (2014) and by Burns (2019), the above drugs as well as amiodarone (which is used for rhythm control) are potentially harmful in those with Wolf-Parkinson-White syndrome and other pre-excitation syndromes in association with AF. As mentioned by Burns (2019), DC cardioversion is generally preferred in these patients in the acute setting, and accessory pathway ablation is recommended by the AHA/ACC/HRS guidelines (2014) as a management option in certain patients
NICE CKS (2020) suggest that clinicians aim for a resting heart rate of 60 to 80 in patients taking rate control, going up to 90-115 bpm during exertion
If required, NICE BNF (n.d.) advise that rate control can be intensified by using the above drugs in combination but if this is not effective then specialist management under cardiology is warranted
In terms of the application of rate control in practice, Gutierrez and Blanchard (2016) note in American Family Physician that rate control is generally used more often than rhythm control, as the constituent drugs have better side effect profiles and there is no need to worry about patients coming out of sinus rhythm, as one would for rhythm control patients

Question 48

rhtyhm contorl AF

Answer 48

DC Cardioversion, which is the use of electrical stimulation to restore sinus rhythm. NICE BNF (n.d.) note that anti-arrhythmic medication or beta-blocker therapy can subsequently be used to maintain sinus rhythm
Amiodarone, which is an antiarrhythmic drug which can restore sinus rhythm on its own. It is suitable in most patients
Flecainide, which is an antiarrhythmic drug that can be used in some patients to restore sinus rhythm, but is contraindicated in those with possible structural or ischaemic heart disease
NICE BNF (n.d.) notes that all of the above methods must be initiated in secondary care. NICE guidelines (2014) also state that the use of cardioversion is an indication for echocardiogram
Patients who are successfully cardioverted are no longer symptomatic but may have a risk of coming out of sinus rhythm and returning to AF. Gutierrez and Blanchard (2016) note that this is can be of concern as maintaining sinus rhythm in certain patients, particularly those over 65, can be a struggle and the medication above can be toxic

Question 49

anticoagulation in AF

Answer 49

Heparin and Low Molecular Weight Heparin (LMWH) are non-oral anticoagulants that are most commonly used in the acute setting over a short length of time or while oral therapy is initiated. Heparin and LMWH are easily cleared by the body, so their anticoagulant effect is lost soon after treatment is stopped
Warfarin is an oral anticoagulant used in certain patients. It requires regular INR monitoring because of its various drug and food interactions, which can mean its anticoagulant effect can be unreliable unless monitored closely. AHA/ACC/HRS guidelines (2014) recommend that doses of warfarin are changed based on these results to achieve an INR of 2-3 for most patients without valve disease, although exact targets may vary based on co-morbidities. Warfarin also needs to be prescribed with LMWH until its anticoagulant effect is established, as it is initially prothrombotic
Direct Oral Anticoagulants (DOACs) are a group of oral anticoagulants including Rivaroxaban, Apixaban and Dabigatran. They are now some of the most commonly used medications in this group. They have a highly predictable and reliable anti-coagulant effect and therefore require reduced blood monitoring compared to warfarin. They do no need to be prescribed with LMWH, but their action is more difficult to reverse

Question 50

relative incidence of idiopathic intracranial HTN [3]

Answer 50

brain tumours 9.5
idiopathic intranial HTN 1
SAH 4.0

Question 51

aetiology of IIH [2]

Answer 51

female, obesity, pregnanct

Question 52

common visual Sx of IIH [5]

Answer 52

Common symptoms:
Headache - 90%
The features of headaches in IIH patients are variable and are not specific to IIH.
They may be intermittent or persistent, occur daily or less frequently.
Nausea and vomiting may occur in association with the headache.
Transient visual obscurations - 70%
These last seconds at a time and can be bilateral or unilateral.
The frequency is variable, ranging from rare or isolated episodes to those occurring several times a day.
The visual obscurations may be associated with changes in position (usually standing) or Valsalva
May be due to transient optic nerve ischaemia
Pulsatile tinnitus - 55%
This symptom in association with a headache is very suggestive of IIH.
Photopsia - 50%
Bright flashes of light that may occur following changes in position, Valsalva, bright light or eye movement.
Back pain - 50%
Retrobulbar pain - 45%

Question 53

physical visual signs of IIH [4]

Answer 53

Papilloedema - 95%
Typically bilateral and symmetric, but may also be asymmetric/unilateral.
Visual field loss - 95%
Typically peripheral , but central visual field can be involved late in the course of disease or earlier if there is concurrent macular disease.
6th nerve palsy
Relative afferent pupillary defect

Question 54

DDx of ICH [4]

Answer 54

n the assessment of an individual with symptoms and signs of increased intracranial pressure, secondary causes of intracranial hypertension must be considered. All of the following can cause symptoms similar to that of IIH:

Intracranial mass lesions (tumor, abscess)
Differences
Tend to affect children and older adults
May cause further focal neurological deficits such as limb weakness/paraesthesia
May cause seizures, fluctuating level of consciousness

Subarachnoid haemorrhage
Differences
Usually sudden onset (thunderclap headache)
May cause further focal neurological deficits such as limb weakness/paraesthesia
May cause seizures, fluctuating level of consciousness

Obstruction of venous outflow, eg, venous sinus thrombosis, jugular vein compression, neck surgery
Differences
Often develops suddenly (thunderclap headache)
May cause further focal neurological deficits such as limb weakness/paraesthesia
May cause seizures, fluctuating level of consciousness

Decreased CSF absorption, eg, arachnoid granulation adhesions after bacterial or other infectious meningitis, subarachnoid hemorrhage
Differences
Past medical history of infectious meningitis/SAH

Malignant systemic hypertension
Differences
Systemic blood pressure >180/120

Question 55

Mx of IIH

Answer 55

Conservative
Weight loss: all overweight patients should be prescribed a low sodium weight reduction programme (IIH Treatment Trial). BMJ Best Practice guidelines suggest that overweight patients should aim to lose 5-10% of total body weight.
Where possible, potentially causative medications such as tetracyclines, retinoids and thyroid replacement therapies, should be stopped.
Regular ophthalmic follow-up with visual field testing is required to assess response to treatment and disease course.

Medical
Acetazolamide is first-line for all patients with visual loss on presentation
Topiramate may be used as an alternative and has the added benefit of causing weight loss in most patients
Refractory cases
loop diuretics may be used
repeated lumbar punctures may be used as a ‘holding’ measure in refractory cases but are not used longer-term
Analgesia: Paracetamol/NSAIDs are recommended first-line for head or back pain.

Surgical
If patients lose vision in spite of maximal medical therapy, surgical treatment by optic nerve sheath fenestration or CSF shunting can be done.

With treatment, there is usually gradual improvement and/or stabilisation, but not necessarily recovery; many patients have persistent papilloedema, elevated intracranial pressure (ICP) and persistent visual field deficits.

Question 56

prognosis of IIH [3]

Answer 56

The visual field loss is due to post-papilloedema optic atrophy.
The peripheries of vision are typically affected first with predominantly nerve fibre bundle type defects.
Symptomatic patients with extensive field loss and severe papilloedema should be considered for a surgical procedure emergently.
Community and clinic-based studies suggest that permanent severe visual loss occurs in about 10% of patients.

Question 57

definition of retroperitoneal

Answer 57

(REH-troh-PAYR-ih-toh-NEE-ul) Having to do with the area outside or behind the peritoneum (the tissue that lines the abdominal wall and covers most of the organs in the abdomen).

Question 58

Abx used in hepatic encephalopathy

Answer 58

such as rifaximin

Question 59

how common is HE in liver cirrhosis pts

Answer 59

More than 40% of people with cirrhosis develop hepatic encephalopathy.[7] More than half of those with cirrhosis and significant HE live less than a year.[1] In those who are able to get a liver transplant, the risk of death is less than 30% over the subsequent five years.[1] The condition has been described since at least 1860

Question 60

what is fetor hepaticus

Answer 60

Fetor hepaticus or foetor hepaticus (Latin, “fetid liver”) (see spelling differences), also known as breath of the dead or hepatic foetor, is a condition seen in portal hypertension where portosystemic shunting allows thiols to pass directly into the lungs. It is a late sign in liver failure and is one of the clinical features of hepatic encephalopathy. Other possible causes are the presence of ammonia and ketones in the breath. The breath has a sweet, fecal smell to it and also described as having the odour of freshly mown ha

Question 61

stages of hepatic encephalopathy

Answer 61

The mildest form of hepatic encephalopathy is difficult to detect clinically, but may be demonstrated on neuropsychological testing. It is experienced as forgetfulness, mild confusion, and irritability. The first stage of hepatic encephalopathy is characterised by an inverted sleep-wake pattern (sleeping by day, being awake at night). The second stage is marked by lethargy and personality changes. The third stage is marked by worsened confusion. The fourth stage is marked by a progression to coma

Question 62

causes of hepatic encephalopathy

Answer 62

Excessive
nitrogen load Consumption of large amounts of protein, gastrointestinal bleeding e.g. from esophageal varices (blood is high in protein, which is reabsorbed from the bowel), kidney failure (inability to excrete nitrogen-containing waste products such as urea), constipation
Electrolyte or
metabolic disturbance Hyponatraemia (low sodium level in the blood) and hypokalaemia (low potassium levels)—these are both common in those taking diuretics, often used for the treatment of ascites; furthermore alkalosis (decreased acid level), hypoxia (insufficient oxygen levels), dehydration
Drugs and
medications Sedatives such as benzodiazepines (often used to suppress alcohol withdrawal or anxiety disorder), narcotics (used as painkillers or drugs of abuse), antipsychotics, alcohol intoxication
Infection Pneumonia, urinary tract infection, spontaneous bacterial peritonitis, other infections
Others Surgery, progression of the liver disease, additional cause for liver damage (e.g. alcoholic hepatitis, hepatitis A)
Unknown In 20–30% of cases, no clear cause for an attack can be found

Question 63

which procedure can induce hepatic encephalopathy

Answer 63

Hepatic encephalopathy may also occur after the creation of a transjugular intrahepatic portosystemic shunt (TIPS)

Question 64

diet for hepatic encephalopathy

Answer 64

In the past, it was thought that consumption of protein even at normal levels increased the risk of hepatic encephalopathy. This has been shown to be incorrect. Furthermore, many people with chronic liver disease are malnourished and require adequate protein to maintain a stable body weight. A diet with adequate protein and energy is therefore recommended.[4][9]

Dietary supplementation with branched-chain amino acids has shown improvement of encephalopathy and other complications of cirrhosis.[4][9]

Some studies have shown benefit of administration of probiotics (“healthy bacteria”)

Question 65

Laxatives for hepatic encephalopathy

Answer 65

Lactulose and lactitol are disaccharides that are not absorbed from the digestive tract. They are thought to decrease the generation of ammonia by bacteria, render the ammonia inabsorbable by converting it to ammonium (NH4+) ions, and increase transit of bowel content through the gut. Doses of 15-30 mL are typically administered three times a day; the result is aimed to be 3–5 soft stools a day, or (in some settings) a stool pH of <6.0.[4][8][9][17] Lactulose may also be given by enema, especially if encephalopathy is severe.[17] More commonly, phosphate enemas are used. This may relieve constipation, one of the causes of encephalopathy, and increase bowel transit.[4]

Lactulose and lactitol are beneficial for treating hepatic encephalopathy, and are the recommended first-line treatment.[4][21] Lactulose does not appear to be more effective than lactitol for treating people with hepatic encephalopathy.[21] Side effects of lactulose and lactitol include the possibility of diarrhea, abdominal bloating, gassiness, and nausea.[21] In acute liver failure, it is unclear whether lactulose is beneficial. The possible side effect of bloating may interfere with a liver transplant procedure if required

Question 66

medications for orthostatic hypotension

Answer 66

The medication midodrine can benefit people with orthostatic hypotension,[30][32] The main side effect is piloerection (“goose bumps”).[32] Fludrocortisone is also used, although based on more limited evidence

Question 67

Sx of headache in ICH

Answer 67

Headache
Tinnitus
Changes in vision

Question 68

what is the Chid-Pugh score? [2]

Answer 68

is used to assess the prognosis of chronic liver disease, mainly cirrhosis

Question 69

Medical uses for ursodeoxycholic acid

Answer 69

UDCA has been used as medical therapy in gallstone disease (cholelithiasis) and for biliary sludge.[8][9] UDCA helps reduce the cholesterol saturation of bile and leads to gradual dissolution of cholesterol-rich gallstones

Question 70

Fragility fractures

Answer 70

Fragility fracture is a type of pathologic fracture that occurs as a result of an injury that would be insufficient to cause fracture in a normal bone.[2] There are three fracture sites said to be typical of fragility fractures: vertebral fractures, fractures of the neck of the femur, and Colles fracture of the wrist. This definition arises because a normal human being ought to be able to fall from standing height without breaking any bones, and a fracture, therefore, suggests weakness of the skeleton.

Question 71

Pathological fractures

Answer 71

Pathological fractures present as a chalkstick fracture in long bones, and appear as a transverse fractures nearly 90 degrees to the long axis of the bone. In a pathological compression fracture of a spinal vertebra fractures will commonly appear to collapse the entire body of vertebra.

Question 72

large bowel obstruction

Answer 72

Small bowel obstructions are most often due to adhesions and hernias

Question 73

small bowel obstruction

Answer 73

while large bowel obstructions are most often due to tumors and volvulus

Question 74

DIfference between large and small bowel obstruction

Answer 74

In small bowel obstruction, the pain tends to be colicky (cramping and intermittent) in nature, with spasms lasting a few minutes. The pain tends to be central and mid-abdominal. Vomiting may occur before constipation.[9]

In large bowel obstruction, the pain is felt lower in the abdomen and the spasms last longer. Constipation occurs earlier and vomiting may be less prominent. Proximal obstruction of the large bowel may present as small bowel obstructio

Question 75

features of nephrotic syndrome

Answer 75

Nephrotic syndrome is characterized by large amounts of proteinuria (>3.5 g per 1.73 m2 body surface area per day,[6] or > 40 mg per square meter body surface area per hour in children), hypoalbuminemia (< 3.5 g/dl), hyperlipidaemia, and edema that begins in the face

Question 76

features of nephrotic syndrome

Answer 76

1. Proteinuria (> 3g/24hr) causing
2. Hypoalbuminaemia (< 30g/L) and
3. Oedema

Question 77

Cause of nephrotic syndrome

Answer 77

Primary glomerulonephritis accounts for around 80% of cases
Minimal change glomerulonephritis (causes 80% in children, 30% in adults)
Membranous glomerulonephritis
Focal segmental glomerulosclerosis
Membranoproliferative glomerulonephritis

Systemic disease (about 20%)
Diabetes mellitus
Systemic lupus erythematosus
Amyloidosis

Drugs
Gold (sodium aurothiomalate), penicillamine

Others
Congenital
Neoplasia: carcinoma, lymphoma, leukaemia, myeloma
Infection: bacterial endocarditis, hepatitis B, malaria

Question 78

what leads to proteinuria

Answer 78

very highh elvels of protein in the urine [proteinuria], low levels protein in the blood, swelling especially around the eyes/feet/hands

Question 79

what is a pathological fracture?

Answer 79

A pathologic fracture is a bone fracture caused by weakness of the bone structure that leads to decrease mechanical resistance to normal mechanical loads.[1] This process is most commonly due to osteoporosis, but may also be due to other pathologies such as cancer, infection (such as osteomyelitis), inherited bone disorders, or a bone cyst. Only a small number of conditions are commonly responsible for pathological fractures, including osteoporosis, osteomalacia, Paget’s disease, Osteitis, osteogenesis imperfecta, benign bone tumours and cysts, secondary malignant bone tumours and primary malignant bone tumours.

Question 80

acute treatment for migraines

Answer 80

an oral triptan and an NSAID, or
an oral triptan and paracetamol

Question 81

chronic Tx for migraines

Answer 81

propranolol
topiramate: should be avoided in women of childbearing age as it may be teratogenic and it can reduce the effectiveness of hormonal contraceptives
amitriptyline

Question 82

RFs for gout

Answer 82

Gender
Men are more likely to develop gout.
A woman’s risk of gout increases following the menopause.
Age
Most commonly, the first attack of gout occurs between the ages of 30 and 50.
Risk increases with age.
Diet
A diet high in purines includes foods such as meat, seafood and fructose-containing foods.
These purines are metabolised to uric acid in the body and so increased consumption of such foods increases the risk of gout.
Alcohol - much like diet, the role of alcohol in gout is linked to purine metabolism.
Metabolic syndrome
Medications associated with increased risk of gout:
Loop and thiazide diuretics
Low dose aspirin
Levodopa
Chronic kidney disease
Physiologically, the kidneys flush out uric acid. If kidneys are impaired, uric acid will build up in the body.
The reverse also happens that persistently high serum uric acid damage the kidneys.

Question 83

purines in diet for gout [3]

Answer 83

Purines are obtained from the diet. This is why diet plays a large role in management - reduced purines = reduced serum uric acid = reduced risk for gout. Dietary items high in purines include:
Alcohol
Red meat
Organ meat e.g. liver/kidney.
Sweetened beverages due to their fructose content (a precursor for purines).

Question 84

how do purines work? [2]

Answer 84

Purines play an important role in serum uric acid balance. They are metabolised into uric acid via a multi-step pathway involving the enzyme xanthine oxidase hence the efficacy of the use of allopurinol (a xanthine oxidase inhibitor) as prophylactic treatment for gout.

Question 85

Where does gout commonly occur? [1]

Answer 85

In contrast to many forms of arthritis, gout develops rapidly reaching maximal severity within 24 hours, and resolves within 5-15 days. Rarely, gout symptoms may appear gradually. 70% of first presentations involve the first MTP however gout may affect other peripheral joints including:
Other joints of the feet, ankle and knee
Joints of the hand, wrist and elbow.
It rarely affects more central joints such as hip and spine.

Question 86

Crystals in gout vs pseudogout

Answer 86

Crystals Gout Pseudogout
Birefringence Negatively birefringent Positively birefringent
Shape Needle shaped Rhomboidal
Crystal type Monosodium urate Calcium pyrophosphate

Question 87

how can pseudogout be confused with gout? [2]

Answer 87

Pseudogout
Pseudogout presents very similarly to gout but few clinical features differentiate the two:
Pseudogout is more likely to affect larger joints such as the knee .
Pseudogout is more likely in the elderly.
It typically presents with a less intense pain.
Chondrocalcinosis may be identified on x-ray.
It is definitively distinguished by rhomboid shaped positively birefringent calcium pyrophosphate crystals in the synovial fluid but often this is not a feasible test.

Question 88

how can RA be confused with gout

Answer 88

Chronic gout may be confused with RA despite mono-articular RA being rare. Distinguishing features include:
The onset of pain in RA is usually more gradual than gout.
Rheumatoid nodules may be present however are easily confused with tophi.
If patient experiences recurrent flares, this is more suggestive of gout.
Rheumatoid factor may be present in both RA and gout so is not useful to distinguish the two. Anti-CCP is much more specific for RA but has relatively low sensitivity.
Synovial fluid analysis would show inflammation in RA but no MSU crystals which would be present in gout.

Question 89

Mx of gout

Answer 89

Management includes:
Self-care - patient should be advised to keep joint elevated to reduce inflammation, limit any trauma to joint and keep it cool (consider using an ice-pack)
Prescription of either of the first line treatments recommended by NICE: colchicine or NSAIDs such as indomethacin. Choice is based on patient preference, renal function and any co-morbidities.
Aspirin is not indicated as it may increase uric acid levels. This is because it prevents excretion of uric acid from the kidneys.
Aspirin may be prescribed in cases of cardiovascular disease and stroke as the benefits outweigh the risk of potentially inducing a gout flare.
Corticosteroids:
A short course of oral corticosteroids such as prednisolone may be used if a patient cannot tolerate NSAIDs.
Intra-articular corticosteroids can also be used.

Question 90

when can allopurinol be used for gout? [2]

Answer 90

EULAR recommends allopurinol as the first-line urate lowering therapy with target uric acid levels of 360µmol/L or less.
It is a xanthine oxidase inhibitor metabolising xanthine to uric acid. This results in reduced deposition of MSU crystals in joints hence the application for gout.
It is generally well tolerated but side effects may include:
Common side-effects - skin rash (may indicate Stevens-Johnson Syndrome) and joint paint/swelling
Rare side effects - drug hypersensitivity syndrome (signs include eosinophilia, lymphadenopathy, fever and multi-organ involvement)
NOTE Allopurinol should not be commenced during an acute attack as it may worsen it and so should be started 1-2 weeks after an acute attack. As it may also precipitate another acute attack, the British Society for Rheumatology recommends prophylactic colchicine (or NSAID if colchicine not tolerated) should be prescribed alongside for up to six months to avoid this.

Question 91

what is the second line treatment for gout and why is it used? [2]

Answer 91

Second-line therapy is febuxostat and is used for those who do not tolerate allopurinol.
It is a non-purine xanthine oxidase inhibitor.
Check liver function prior to commencing treatment.

Question 92

tophi, bone and renal compications of gout

Answer 92

As mentioned previously, tophi form when MSU crystals deposit to form hard lumps. They can form in tissues, bone and cartilage and if large and painful may impact a patients ability to perform daily tasks.
Tophi are usually a sign of chronic gout, their presence indicates that there are likely to be MSU crystal deposits elsewhere in the body.
Bone complications
Repeated attacks of gout and the presence of tophi all contribute to bone erosion and weakening of joints resulting in degenerative arthritis. In the most serious of cases, surgery will be required to rectify this damage.
A 2018 population-based study found that gout conferred a 20% increased risk of osteoporosis.
Renal complications
Kidney stones may occur due to deposits of MSU crystals in the urinary tract as a result of hyperuricaemia. They can disrupt the flow of urine, cause pain and make the patient more susceptible to an infection of the urinary tract or kidney.
Although kidney disease is a risk factor for gout, gout can also cause kidney disease. Although not fully understood, it is believed kidney disease may result due to the passage of MSU crystals through kidneys causing scarring. This scarring then reduces functionality of the kidneys.

Question 93

Mx for gonorrhoea

Answer 93

IM ceftriaxone 1g

Question 94

what is tumour lysis syndrome

Answer 94

Tumour lysis syndrome (TLS) is a potentially deadly condition related to the treatment of high-grade lymphomas and leukaemias. It can occur in the absence of chemotherapy but is usually triggered by the introduction of combination chemotherapy.

Question 95

Sx and Sx of blood tranfusion reactions

Answer 95

Symptoms

Feeling of apprehension or ‘something wrong’.
Flushing.
Chills.
Pain at the venepuncture site.
Myalgia.
Nausea.
Pain in the abdomen, flank or chest.
Shortness of breath.
Signs

Fever (rise of 1.5°C or more) and rigors.
Hypotension or hypertension.
Tachycardia.
Respiratory distress.
Oozing from wounds or puncture sites.
Haemoglobinaemia.
Haemoglobinuria.

Question 96

acute haemolytic reactions

Answer 96

ncompatible transfused red cells react with the patient’s own anti-A or anti-B antibodies or other alloantibodies (eg, anti-rhesus (Rh) D, RhE, Rhc and Kell) to red cell antigens. Complement can be activated and may lead to disseminated intravascular coagulation (DIC).
Infusion of ABO incompatible blood almost always arises from errors in labelling sample tubes/request forms or from inadequate checks at the time of transfusion. Where red cells are mistakenly administered, there is about a 1 in 3 risk of ABO incompatibility and 10% mortality with the severest reaction seen in a group O individual receiving group A red cells.
Non-ABO red cell antibody haemolytic reactions tend to be less severe but the Kidd and Duffy antigens also activate complement and can cause severe intravascular haemolysis.

Question 97

infective shock transfusion reactions

Answer 97

Bacterial contamination of a blood component is a rare but severe and sometimes fatal cause of transfusion reactions.
Acute onset of hypertension or hypotension, rigors and collapse rapidly follows the transfusion.
No UK cases of bacterial contamination of blood products were confirmed by SHOT in 2020[2].
Platelets are more likely to be associated with bacterial contamination than red cells, as they are stored at a higher temperature.

Question 98

TRALI transfusion

Answer 98

TRALI is a form of acute respiratory distress due to donor plasma containing antibodies against the patient’s leukocytes.
Transfusion is followed within six hours of transfusion by the development of prominent nonproductive cough, breathlessness, hypoxia and frothy sputum[6]. Fever and rigors may be present.
CXR shows multiple perihilar nodules with infiltration of the lower lung fields.
Implicated donors are usually multiparous women (who are more likely to have become alloimmunised) and should be removed from the blood panel where possible. Gas exchange was significantly worse after transfusion of female but not male donor blood products in one study of high plasma volume transfusions in the critically ill

Question 99

inflammatory arthritis signs

Answer 99

Pain in the morning
Systemic features
Raised inflammatory markers

Question 100

pain in side of thigh

Answer 100

Due to repeated movement of the fibroelastic iliotibial band
Pain and tenderness over the lateral side of thigh
Most common in women aged 50-70 years

Question 101

pain in side of thigh

Answer 101

Caused by compression of lateral cutaneous nerve of thigh
Typically burning sensation over antero-lateral aspect of thigh

Question 102

what is diabetes insipidus

Answer 102

Diabetes insipidus (DI) is a condition characterised by either a decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI).

Question 103

diabetes insipidus

Answer 103

high plasma osmolality, low urine osmolality
a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
water deprivation test

Question 104

Causes of diabetes insipidus

Answer 104

Causes of cranial DI
idiopathic
post head injury
pituitary surgery
craniopharyngiomas
infiltrative
histiocytosis X
sarcoidosis
DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)
haemochromatosis

Causes of nephrogenic DI
genetic:
more common form affects the vasopression (ADH) receptor
less common form results from a mutation in the gene that encodes the aquaporin 2 channel
electrolytes
hypercalcaemia
hypokalaemia
lithium
lithium desensitizes the kidney’s ability to respond to ADH in the collecting ducts
demeclocycline
tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis