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MRCP p1 > General deck > Flashcards

General deck Flashcards

1
Q

What are the features of myotonic dystrophy? (DM -1)

A

Dystrophia myotonica - DM1
distal weakness initially
autosomal dominant
diabetes
dysarthria

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2
Q

What are the symptoms of behchet’s disease?

A

classic triad of symptoms are oral ulcers, genital ulcers and anterior uveitis

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3
Q

What is seen on immunofluorescence of the skin biopsy in bullous pemphegoid?

A

linear IgG and/or linear c3 staining along the basement zone is present in greater than 90% of cases.

bu(LL)ous pemphi(G)oid: auto-immune skin blistering
Linear IgG
Linear c3

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4
Q

What is the pathophysiology behind hereditary angio-oedema?

A

Autosomal dominant conditon
associated with low plasma levels of C1 inhibitor protein
C1-INh is a multifunactional serine protease inhibitor- the probable mechanism behind attacks in uncontrolled release of bradykinin resulting in oedema of tissue.

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5
Q

What is the investigation used to diagnose hereditary angio-oedema?

A

C1-INH level is low during an attack
low C2 and C4 levels are seen, even between attacks. Serum C4 is the most reliable and widely used screening tool

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6
Q

What is the treatment of acute hereditary angio-oedema

A

IV C1-inhibitor concentrate, fresh frozen plasma (FFP) if this is not available

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7
Q

What is the prophylactic tx of hereditary angio-oedema ?

A

Anabolic steroid - Danazol

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8
Q

What are the things to monitor while giving magnesium sulphate in patients with pre-eclampsia?

A

urine output, reflexes, respiratory rate and oxygen saturations should be monitored during treatment

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9
Q

How is respiratory depression in pre-eclampsia treated?

A

Calcium gluconate is the first-line treatment for magnesium sulphate induced respiratory depression

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10
Q

Which viral meningitis causes low CSF glucose?

A

Mumps virus
herpes encephalitis

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11
Q

What is the classical trend seen on CSF with bacterial infection?

A

Cloudy appearance
Low glucose (<1/2)
Protein is high
High neutrophils

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12
Q

What is the classical trend seen on CSF with viral infections?

A

Clear appearance
60-80% of normal glucose
Normal or raised protein
high lymphocytes

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13
Q

What is the classical trend seen on CSF with TB infections?

A

Slight cloudy, fibrin web
Low glucose
High protein
Mildly raised lymphocytes

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14
Q

How would you differentiate NMS and serotonin syndrome based on symptoms?

A

Myoclonus is characteristic of serotonin syndrome
Rigidity is typical of NMS

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15
Q

What is the blood film characteristic of hyposplenism?

A

Howell-Jolly bodies and siderocytes

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16
Q

What are the indications of LTOT?

A

LTOT should be offered to:

patients with a pO2 of < 7.3 kPa or to those with a pO2 of 7.3 - 8 kPa and one of the following:
- secondary polycythaemia
- nocturnal hypoxaemia
- peripheral oedema
- pulmonary hypertension

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17
Q

What are the features of patients with COPD who have asthmatic/steroid responsiveness?

A
  • any previous, secure diagnosis of asthma or of atopy
  • a higher blood eosinophil count: note that NICE recommend a full blood count for all patients as part of the work-up
  • substantial variation in FEV1 over time (at least 400 ml)
  • substantial diurnal variation in - peak expiratory flow (at least 20%)
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18
Q

Which COPD patients are good candidates to be on azithromycin ?

A
  • patients should not smoke, have optimised standard treatments and continue to have exacerbations
  • Should have had CT thorax to exclude bronchiectasis and sputum culture to rule out atypical infections and tuberculosis
  • LFTs and an ECG to exclude QT prolongation should be done as azithromycin can prolong QT interval
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19
Q

What are interventions that can improve survival of stable COPD patients?

A
  1. smoking cessation - the single most important intervention in patients who are still smoking
  2. long term oxygen therapy in patients who fit criteria
  3. lung volume reduction surgery in selected patients
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20
Q

What are the various serotonin (5-HT) medications and which receptors do they work on?

A

5-HT1 –> triptan/ergot –> agonist
5-HT2 –> Atypical antipsychotics/Cyproheptadine /pizotifen–> antagonist
5-HT3 –> Ondansetron –> antagonist

5-HT2 and D2 are blocked by antipsychotics [both are 2]

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21
Q

What are the specalised cardiac imaging tools and what do they help diagnose?

A

SPECT scan: myocardial perfusion and myocardial viability

MUGA: LV ejection fraction

Cardiac CT: ischemia heart disease

CMR: structure of heart

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22
Q

What are the drugs that cause cholestasis?

A

-combined oral contraceptive pill
-antibiotics: flucloxacillin, co-amoxiclav, erythromycin*
-anabolic steroids, testosterones
phenothiazines: chlorpromazine, prochlorperazine
-sulphonylureas
-fibrates
-rare reported causes: nifedipine

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23
Q

What are differences in X-ray features between rheumatoid and osetoarthritis?

A

arthritis = LOSS
OA - loss of joint space, ostephytes, subchondrial sclerosis, subchondrial cysts

RA - Loss of joint space, Osteoporosis (juxta-articular), soft tissue swelling, subluxation (later with erosions)

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24
Q

When do you suspect thalassemia in microcytic anaemia picture?

A

Mentzer index :

The index is calculated from the results of a complete blood count. If the quotient of the mean corpuscular volume (MCV, in fL) divided by the red blood cell count (RBC, in Millions per microLiter) is less than 13, thalassemia is said to be more likely. If the result is greater than 13, then iron-deficiency anemia is said to be more likely

Mentzer index = MCV/RBC .if less then 13 = Thalassemia

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25
Q

what are the causes of type 1 membranoproliferazive glomerulonephritis?

A

Immunoglobulin (IG)-mediated membranoproliferative glomerulonephritis (type 1 MPGN)

cryoglobulinaemia, hepatitis C

Associated with SLE, monoclonal gammopathy

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26
Q

What do you see on renal biopsy of type 1 membranoproliferative glomerulonephritis?

A

subendothelial and mesangium immune deposits of electron-dense material resulting in a ‘tram-track’ appearance

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27
Q

what is the pathophysiology and causes of type 2 membranoproliferazive glomerulonephritis?

A

Complement-mediated membranoproliferative glomerulonephritis

Associated with dense deposit disease (IgG antibodies that stabilize C3 convertase, i.e., C3 nephritic factor, cause a persistent complement activation, leading to a depletion of C3)

causes: partial lipodystrophy (patients classically have a loss of subcutaneous tissue from their face), factor H deficiency

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28
Q

What are membranoproliferative glomerulonehritis associated with?

A

-Both associated with HBV, HCV, and cryoglobulinemia
-Hereditary diseases (e.g., sickle cell disease, α1-antitrypsin deficiency) [13]
-Drugs (e.g., heroin, α-interferon)
-Tumors (e.g., lymphoma)
-Autoimmune diseases (e.g., SLE)

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29
Q

What are the characteristic clinical and microscopic features of type 2 membranoproliferative glomerulonephritis?

A
  • Intramembranous C3 deposits (dense deposit disease) on basement membrane
  • ↓ Serum C3 complement levels
  • C3b nephritic factor is found in 70%
    an antibody to alternative-pathway C3 convertase (C3bBb)
    stabilizes C3 convertase

causes: partial lipodystrophy (patients classically have a loss of subcutaneous tissue from their face), factor H deficiency

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30
Q

What is the adjuvant tx for T1DM and when is it used?

A

Metformin should be considered in addition to insulin therapy for adults with type 1 diabetes if they have a BMI of 25 kg/m2 or above (23 kg/m2 or above for people from South Asian and related family backgrounds)

This is because overweight and obese patients will also likely have a degree of insulin resistance.

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31
Q

What are the target BPs for pts with T1DM and how is it treated?

A

In adults with type 1 diabetes, blood pressure targets are governed by urine albumin:creatinine ratio (ACR) as follows:

  • For adults with an ACR less than 70 mg/mmol, aim for a clinic systolic blood pressure less than 140 mmHg (target range 120 to 139 mmHg) and a clinic diastolic blood pressure less than 90 mmHg.
  • For adults with an ACR of 70 mg/mmol or more, aim for a clinic systolic blood pressure less than 130 mmHg (target range 120 to 129 mmHg) and a clinic diastolic blood pressure less than 80 mmHg.
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32
Q

Which drugs cause gynacomasteria?

A

spironolactone (most common drug cause)
cimetidine
digoxin
cannabis
finasteride
GnRH agonists e.g. goserelin, buserelin
oestrogens, anabolic steroids

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33
Q

what are some examples of medications that act on IL1?

A

Anakinra: IL-1 receptor antagonist
used in the management of rheumatoid arthritis

Canakinumab: monoclonal antibody targeted at IL-1 beta
used systemic juvenile idiopathic arthritis and adult-onset Still’s disease

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34
Q

How does carbamezapine work?

A

binds to sodium channels increases their refractory period

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35
Q

What are the adverse effects of carbamazepine?

A

P450 enzyme inducer
dizziness and ataxia
drowsiness
headache
visual disturbances (especially diplopia)
Steven-Johnson syndrome
leucopenia and agranulocytosis
hyponatraemia secondary to syndrome of inappropriate ADH secretion

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36
Q

What is the mode of inheritance of hereditary haemorrhagic telengeictasisa?

A

Autosomal dominant

epistaxis: spontaneous, recurrent nosebleeds
telangiectasies : lips, oral cavity, fingers and nose
Visceral lesions: gastrointerinal telegeictasisa, pulmonary AVM

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37
Q

What are the features of fabry’s disease?

A

FABRY’C disease:
F - foggy lens
A - angiokeratomas
B - burning pain
R - renal failure
Y - youth death
C - CV malformation

x- linked recessive
deficiency of alpha-galactosidase A

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38
Q

What secondary messengers can be produced by adrenaline, No and acetylcholine?

A

A-drenaline -> cyclic A-mp
Nitric oxide: cGmp
AcetyLcholine: L-igand gated

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39
Q

what are the indications for immediate valvular surgery in patients with endocarditis?

A

severe valvular incompetence
aortic abscess (often indicated by a lengthening PR interval)
infections resistant to antibiotics/fungal infections
cardiac failure refractory to standard medical treatment
recurrent emboli after antibiotic therapy

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40
Q

what is the components of R-CHOP?

A

R-CHOP which consists of rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone

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41
Q

how does cyclophosphamide function?

A

alkylating agent that promotes cross-linking of DNA.

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42
Q

how does vincristine function?

A

Inhibition of microtubule formation is the mechanism of drugs

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43
Q

how does doxurubicin function?

A

Inhibition of topoisomerase II and DNA/RNA synthesis

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44
Q

what are the side effects of cyclophosphamide?

A

Haemorrhagic cystitis, myelosuppression, transitional cell carcinoma

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45
Q

what syphilis test can you use to check if soemone’s treated for syphilis has reinfection?

A

Rapid plasma reagin test (RPR) or VDRL - non-treponema specific
based upon the reactivity of serum from infected patients to a cardiolipin-cholesterol-lecithin antigen
assesses the quantity of antibodies being produced
becomes negative after treatment

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46
Q

what are the causes of false positive increases in non-treponemal tests?

A

pregnancy
SLE, anti-phospholipid syndrome
tuberculosis
leprosy
malaria
HIV

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47
Q

what is seen on biospy of gastric cancer?

A

signet ring cells may be seen in gastric cancer. They contain a large vacuole of mucin which displaces the nucleus to one side. Higher numbers of signet ring cells are associated with a worse prognosis

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48
Q

what is the side effect seen when vancomycin is administered too quickly?

A

red man syndrome; occurs on rapid infusion of vancomycin

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49
Q

what are some of the side effects of vancomycin?

A

nephrotoxicity
ototoxicity
thrombophlebitis
red man syndrome; occurs on rapid infusion of vancomycin

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50
Q

what are some of the common signs of pneumococcal pneumonia?

A

rapid onset
high fever
pleuritic chest pain
herpes labialis (cold sores)

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51
Q

what are the haematological features of lead poisioning?

A

full blood count: microcytic anaemia. Blood film shows red cell abnormalities including basophilic stippling and clover-leaf morphology

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52
Q

what is the treatment for lead poisoning?

A

Management - various chelating agents are currently used:
dimercaptosuccinic acid (DMSA)
D-penicillamine
EDTA
dimercaprol

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53
Q

what is ‘egg-shell’ calcification of the hilar lymph nodes on CXR a sign of?

A

Silicosis
upper zone fibrosing lung disease

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54
Q

who is donepezil contraindicated in?

A

contraindicated in patients with bradycardia

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55
Q

what are the 5 As of ankylosing spondylitis

A

Apical fibrosis
Anterior uveitis
Aortic regurgitation
Achilles tendonitis
AV node block
Amyloidosis

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56
Q

what are the common causes of respiratory alkalosis?

A

Common causes
anxiety leading to hyperventilation
pulmonary embolism
salicylate poisoning*
CNS disorders: stroke, subarachnoid haemorrhage, encephalitis
altitude
pregnancy

*salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis. Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst later the direct acid effects of salicylates (combined with acute renal failure) may lead to an acidosis

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57
Q

what are the common causes of livedo reticularis?

A

idiopathic (most common)
polyarteritis nodosa
systemic lupus erythematosus
cryoglobulinaemia
antiphospholipid syndrome
Ehlers-Danlos Syndrome
homocystinuria

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58
Q

what are the features of PAN? (polyarteritis nodosa)

A

fever, malaise, arthralgia
weight loss
hypertension
mononeuritis multiplex, sensorimotor polyneuropathy
testicular pain
livedo reticularis
haematuria, renal failure
perinuclear-antineutrophil cytoplasmic antibodies (ANCA) are found in around 20% of patients with ‘classic’ PAN
hepatitis B serology positive in 30% of patients

medium-sized arteries with necrotizing inflammation leading to aneurysm formation

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59
Q

what are the drugs associated with lung fibrosis?

A

amiodarone
cytotoxic agents: busulphan, bleomycin
anti-rheumatoid drugs: methotrexate, sulfasalazine
nitrofurantoin
ergot-derived dopamine receptor agonists (bromocriptine, cabergoline, pergolide)

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60
Q

what drug allergy can also affect the use of sulfasalazine?

A

allergy to aspirin or sulphonamides (cross-sensitivity)

5-aminosalicylic acid compounds (e.g. mesalazine and sulfasalazine) are a cornerstone of treating ulcerative colitis. However, patients who are allergic to aspirin may also react to 5-aminosalicylic acid compounds as they share structural similarity.

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61
Q

what drugs can cause peripheral neuropathy?

A

amiodarone
isoniazid
vincristine
nitrofurantoin
metronidazole

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62
Q

what drugs can trigger Methaemoglobinaemia?

A

sulphonamides, nitrates (including recreational nitrates e.g. amyl nitrite ‘poppers’), dapsone, sodium nitroprusside, primaquine

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63
Q

when do you suspect methaemaglobinaemia clinically?

A

‘chocolate’ cyanosis
dyspnoea, anxiety, headache
severe: acidosis, arrhythmias, seizures, coma
normal pO2 but decreased oxygen saturation

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64
Q

what is the mechanism of action of flurouracil?

A

Pyrimidine analogue inducing cell cycle arrest and apoptosis by blocking thymidylate synthase (works during S phase)

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65
Q

what are the variants of protozoa that cause cyrptosporiadiasis?

A

Cryptosporidium hominis
Cryptosporidium parvum

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66
Q

how is the diagnosis of cryptosporadiasis made?

A

stool: modified Ziehl-Neelsen stain (acid-fast stain) of the stool may reveal the characteristic red cysts of Cryptosporidium

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67
Q

what is the management of cryptosporadiasis entail?

A
  • is largely supportive for immunocompetent patients
  • if the patient has HIV and is not on antiretroviral therapy then this should be started and often will be enough to resolve the infection
  • nitazoxanide may be used for immunocompromised patients
  • rifaximin is also sometimes used for immunocompromised patients/patients with severe disease
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68
Q

what is the treatment for leptospirosis?

A

high-dose benzylpenicillin or doxycycline

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69
Q

what is the diagnostic testing for leptospirosis?

A
  • serology: antibodies to Leptospira develop after about 7 days
  • PCR
  • culture
    1. growth may take several weeks so limits usefulness in diagnosis
    2. blood and CSF samples are generally positive for the first 10 days
    3. urine cultures become positive during the second week of illness
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70
Q

what is the cause of leptospirosis?

A

spirochaete Leptospira interrogans (serogroup L. icterohaemorrhagiae)

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71
Q

what are the features of leptospirosis?

A

The early phase is due to bacteraemia and lasts around a week:
- may be mild or subclinical
- fever
- flu-like symptoms
- subconjunctival suffusion (redness)/haemorrhage

Second immune phase may lead to more severe disease (Weil’s disease):
- acute kidney injury (seen in 50% of patients)
- hepatitis: jaundice, hepatomegaly
- aseptic meningitis

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72
Q

what are the side effects of the second line diabetic medications?

A

Sulphonylureas e.g. gliclazide. Side effects include weight gain and hypoglycaemia.

Gliptin’s e.g. sitagliptin. Side effects include headaches, but are generally well tolerated.

Thiazolidinedione e.g. pioglitazone. Side effects include fluid retention and weight gain.

Sodium/glucose cotransporter 2 (SGLT-2) inhibitors e.g. canagliflozin. Side effects include urinary tract infections and increased risk of foot amputations (mainly with canagliflozin, but no evidence of a link with empagliflozin and dapagliflozin).

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73
Q

what are features that suggest steroid responsiveness in COPD patients?

A
  • previous diagnosis of asthma or atopy
  • a higher blood eosinophil count
  • substantial variation in FEV1 over time (at least 400 ml)
  • substantial diurnal variation in peak expiratory flow (at least 20%)
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74
Q

what is the pathophysiology behind heparin induced thrombocytopenia?

A

immune mediated - antibodies form against complexes of platelet factor 4 (PF4) and heparin

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75
Q

what does mutation in p53 gene cause?

A

Mutations in the p53 gene result in a high risk of developing invasive cancer (about 50% by age 30 and 90% by age 70), particularly early-onset breast cancer, sarcoma, brain tumours (particularly glioblastoma), leukaemia and adrenocortical carcinoma.

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76
Q

what are the medications which cause impaired glucose tolerance?

A

STATIN:

Steroids
Thiazides
Antipsychotics
Tacrolimus/ciclosporin
Interferon-alpha
Nicotinic acid

TASTINg Sugar( impared glucose tolerance)

Thiazides, Antiphychotics, Steroids, T cell in inhibitors(tacrolimus |&| cyclosporin), interferon alpha, nicotinic acid.
Sugar = impared glucose tolerance

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77
Q

what is internuclear ophthalmoplegia?

A

impaired adduction of the eye on the same side as the lesion
horizontal nystagmus of the abducting eye on the contralateral side

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78
Q

what is a strong sign of ocular involvement in herpes zoster infections?

A

Hutchinson’s sign: rash on the tip or side of the nose. Indicates nasociliary involvement and is a strong risk factor for ocular involvement

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79
Q

what are the features of mcardle disease?

A

McArdle …….. M muscle C cramps
After huRDLEs (after exercise)

M= Muscle pain
C=cramps
Ar=autosomal recessive
D=deficiency of myophosphorylase
L=low lactate levels
E=exercise related

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80
Q

what are the culture negative causes of endocarditis?

A

prior antibiotic therapy
Coxiella burnetii
Bartonella
Brucella
HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)

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81
Q

what are the T score ranges to diagnose oseteoporosis or osetopenia?

A

> -1.0 = normal
-1.0 to -2.5 = osteopaenia
< -2.5 = osteoporosis

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82
Q

what is Lesch-Nyhan syndrome?

A
  • hypoxanthine-guanine phosphoribosyl transferase (HGPRTase) deficiency
  • x-linked recessive therefore only seen in boys
  • features: gout, renal failure, neurological deficits, learning difficulties, self-mutilatio
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83
Q

what are the risk factors for developing eosinophilic oesophagitis?

A

Allergies/ asthma: suffering from food/ environmental allergies or atopic dermatitis and asthma increases the risk of diagnosis
Male sex
Family history of eosinophilic oesophagitis or allergies
Caucasian race
Age between 30-50
Coexisting autoimmune disease e.g. coeliac disease

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84
Q

How do you differentiate VT from SVT with aberrant conduction?

A

AV dissociation
fusion or capture beats
positive QRS concordance in chest leads
marked left axis deviation
history of IHD
lack of response to adenosine or carotid sinus massage
QRS > 160 ms

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85
Q

what is the mode of function of varenicline?

A

a nicotinic receptor partial agonist

should be started 1 week before the patients target date to stop
the recommended course of treatment is 12 weeks (but patients should be monitored regularly and treatment only continued if not smoking)

has been shown in studies to be more effective than bupropion

nausea is the most common adverse effect. Other common problems include headache, insomnia, abnormal dreams

varenicline should be used with caution in patients with a history of depression or self-harm. There are ongoing studies looking at the risk of suicidal behaviour in patients taking varenicline
contraindicated in pregnancy and breast feeding

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86
Q

what are the common causes of erythema multiforme?

A

viruses: herpes simplex virus (the most common cause), Orf*
idiopathic
bacteria: Mycoplasma, Streptococcus
drugs: penicillin, sulphonamides, carbamazepine, allopurinol, NSAIDs, oral contraceptive pill, nevirapine
connective tissue disease e.g. Systemic lupus erythematosus
sarcoidosis
malignancy

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87
Q

what is the cause of anthrax?

A

Bacillus anthracis, a Gram positive rod.
Bacillus anthracis produces a tripartite protein toxin
1. protective antigen
2. oedema factor: a bacterial adenylate cyclase which increases cAMP
3. lethal factor: toxic to macrophages

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88
Q

what is the treatment for antharax?

A

the current Health Protection Agency advice for the initial management of cutaneous anthrax is ciprofloxacin

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89
Q

what are the different genes affected in inherited colon cancer conditions?

A

APC - adenomatous polyposis coli (APC) gene in Familial adenamotous polyposis

HNPCC (Lynch syndrome), an autosomal dominant condition, is the most common form of inherited colon cancer. Around 90% of patients develop cancers, often of the proximal colon, which are usually poorly differentiated and highly aggressive.
- MSH2 gene - HNPCC
- MLH 1 gene - non-polyposis colorectal carcinoma (HNPCC)

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90
Q

what is the amsterdam criteria and how is it used?

A

The Amsterdam criteria are sometimes used to aid diagnosis:
1. at least 3 family members with colon cancer
2. the cases span at least two generations
3. at least one case diagnosed before the age of 50 years

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91
Q

what is the amsterdam criteria and how is it used?

A

The Amsterdam criteria are sometimes used to aid diagnosis:
1. at least 3 family members with colon cancer
2. the cases span at least two generations
3. at least one case diagnosed before the age of 50 years

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92
Q

what is the treatment for aortic dissection types?

A

Aortic dissection
type A - ascending aorta - control BP (IV labetalol) + surgery
surgical management, but blood pressure should be controlled to a target systolic of 100-120 mmHg whilst awaiting intervention

type B - descending aorta - control BP(IV labetalol)

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93
Q

what is the most common inherited bleeding disorder and what is the most common inherited thrombophilia?

A

VWF disease - inherited bleeding disorder
Activated protein C resitance - most common inherited thrombophilia

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94
Q

what is the typical causes of membranous nephropathy?

A

Primary: anti-PLA2R antibodies
Secondary:
-Infections (HBV, HCV, malaria, syphilis)
- Autoimmune diseases (e.g., SLE)
- Tumors (e.g., lung cancer, prostate cancer)
- Medications (e.g., NSAIDs, penicillamine, gold)

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95
Q

how do you differentiate FSGS vs membranous nephropathy vs membranoproliferatrive glomerulonephritis?

A

membranous nephropathy - Biopsy would show subepithelial immune complex deposits
Granular subepithelial deposits of IgG and C3 (dense deposits) → spike and dome appearance

FSGS:
Light microscopy: segmental sclerosis and hyalinosis

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96
Q

what are the causes of renal tubular acidosis and what are the complications?

A

causes include idiopathic, rheumatoid arthritis, SLE, Sjogren’s, amphotericin B toxicity, analgesic nephropathy

complications include nephrocalcinosis and renal stones

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97
Q

what is the difference in pathology in RTA type 1 vs type 2 vs type 3?

A

type 1: inability to generate acid urine (secrete H+) in distal tubule
The α-intercalated cells of the distal tubule are unable to secrete H+ (apical) → ↓ intracellular production of HCO3-; → ↓ HCO3-/Cl- exchanger activity (basolateral) → decreased concentration of HCO3- in the blood → metabolic acidosis
causes hypokalaemia

Type 2: decreased HCO3- reabsorption in proximal tubule
The proximal convoluted tubule cells are unable to reabsorb HCO3- leading to increased HCO3- excretion in the urine.
H+ secretion from α-intercalated cells in the collecting duct can acidify the urine, but cannot compensate for the excessive HCO3- excretion in the urine, thus resulting in distal tubular acidosis.

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98
Q

what are the causes of type 2 RTA?

A

causes include idiopathic, as part of Fanconi syndrome, Wilson’s disease, cystinosis, outdated tetracyclines, carbonic anhydrase inhibitors (acetazolamide, topiramate)

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99
Q

what are the drug causes of SIADH?

A

sulfonylureas - glimepiride and glipizide
SSRIs, tricyclics
carbamazepine
vincristine
cyclophosphamide

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100
Q

what are features of life threatening asthma?

A

PEFR < 33% best or predicted
Oxygen sats < 92%
‘Normal’ pC02 (4.6-6.0 kPa)
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma

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101
Q

what is the criteria of discharge of asthma?

A

Criteria for discharge
been stable on their discharge medication (i.e. no nebulisers or oxygen) for 12–24 hours
inhaler technique checked and recorded
PEF >75% of best or predicted

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102
Q

how do you manage diabetes in patients with MI?

A

stop oral hypglycaemics and start on IV insulin - sliding scale

Manage hyperglycaemia in patients admitted to hospital for an acute coronary syndrome (ACS) by keeping blood glucose levels below 11.0 mmol/litre while avoiding hypoglycaemia. In the first instance, consider a dose-adjusted insulin infusion with regular monitoring of blood glucose levels.’

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103
Q

what conditions is seborrhic dermatitis associated with?

A

HIV
Parkinson’s disease

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104
Q

what are the ECG changes seen in Subarachnoid haemorrhage?

A

ECG changes including ST elevation may be seen
this may be secondary to either autonomic neural stimulation from the hypothalamus or elevated levels of circulating catecholamines

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105
Q

when do you consider doing a CT head in patients with suspected SAH?

A

if CT head is done within 6 hours of symptom onset and is normal
- new guidelines suggest not doing a lumbar puncture
- consider an alternative diagnosis

if CT head is done more than 6 hours after symptom onset and is normal
do a lumber puncture (LP)
timing wise the LP should be performed at least 12 hours

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106
Q

what is the radiological sign seen with pancreatic cancer?

A

imaging may demonstrate the ‘double duct’ sign - the presence of simultaneous dilatation of the common bile and pancreatic ducts

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107
Q

what is the infection associated with peri-anal itching?

A

Enterobius vermicularis (threadworms)

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108
Q

what is the treatment for campylobacter infections?

A

clarithromycin

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109
Q

what is the treatment for non-specific uretheritis?

A

doxycycline

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110
Q

convert codeine to morphine

A

divide by 10

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111
Q

what is the cause of genital warts?

A

Genital warts - 90% are caused by HPV 6 & 11

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112
Q

who gets screening for familial hypercholestrolaemia ?

A
  • if one parent is affected by familial hypercholesterolaemia, arrange testing in children by age 10
  • if both parents are affected by familial hypercholesterolaemia, arrange testing in children by age 5
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113
Q

what is the pathophysiology of gilbert syndrome?

A

deficiency of UDP glucuronosyltransferase

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114
Q

what are the causes of Lichenoid drug eruptions?

A

gold
quinine
thiazides

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115
Q

what is the diagnostic investigation for budd chiari syndrome?

A

ultrasound with Doppler flow studies is very sensitive and should be the initial radiological investigation

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116
Q

which meds are contraindicated with the use of sildenafil?

A

Nitrates and nicorandil

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117
Q

what are the side effects of phenytoin?

A

common: gingival hyperplasia (secondary to increased expression of platelet derived growth factor, PDGF), hirsutism, coarsening of facial features, drowsiness

megaloblastic anaemia (secondary to altered folate metabolism)
peripheral neuropathy
enhanced vitamin D metabolism causing osteomalacia
lymphadenopathy
dyskinesia

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118
Q

how does mycoplasma pneumoniae cause red blood cell agglutination?

A

Mycoplasma pneumoniae promotes the production of IgM antibodies by the immune system, which bind to red blood cells, causing them to agglutinate with each other. The IgM antibodies are termed cold agglutinins because they are most effective in causing agglutination at lower temperatures.

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119
Q

what are the complications that mycoplasma pneumoniae can cause?

A
  • Cold agglutins - haemolytic anaemia
  • erythema multiforme, erythema nodosum
  • meningoencephalitis
  • bullous myringitis
  • pericarditis/myocarditis
  • gastrointestinal: hepatitis, pancreatitis
  • renal: acute glomerulonephritis
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120
Q

what does TCA over dose present as ? (imipramine, amitryptaline)

A

anticholinergic properties: dry mouth, dilated pupils, agitation, sinus tachycardia, blurred vision.

Features of severe poisoning include:
arrhythmias
seizures
metabolic acidosis
coma

ECG changes include:
sinus tachycardia
widening of QRS
prolongation of QT interval

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121
Q

Pt has known HIV and has come in with coughing and chesty symtoms. CXR shows bilateral hilar shadowing. How are you going to treat? ph 7.41 pO2 8.9 pCO2 3.6

A

Co-trimoxazole

steroids if hypoxic (if pO2 < 9.3kPa then steroids reduce risk of respiratory failure by 50% and death by a third)

IV pentamidine in severe cases

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122
Q

what are the drugs that induce thrombocytopenia?

A

QANADAH

Quinine, abciximab, NSAIDs, Antibiotics.PRS.NOT QRS, Diuretics, Anticonvulsants..VC, Heparin

antibiotics: penicillins, sulphonamides, rifampicin
anticonvulsants: carbamazepine, valproate

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123
Q

what are the signs of ankylosing spondylotis?

A
  • sacroiliitis: subchondral erosions, sclerosis
  • squaring of lumbar vertebrae
    ‘bamboo spine’ (late & uncommon)
  • syndesmophytes: due to ossification of outer fibers of - annulus fibrosus
    chest x-ray: apical fibrosis
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124
Q

why is doxycycline preferred to azithromycin in chlamydia?

A

. Doxycycline is the preferred antibiotic as patients with Chlamydia are at higher risk of co-infection with Mycoplasma genitalium,

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125
Q

which clotting factor is raised in liver disease?

A

In liver failure all clotting factors are low, except for factor VIII which is paradoxically supra-normal. This is because factor VIII is synthesised in endothelial cells throughout the body, unlike the other clotting factors which are synthesised purely in hepatic endothelial cells. Furthermore, whilst activated factor VIII is usually rapidly cleared from the blood stream, good hepatic function is required for this to occur, further leading to increases in circulating factor VIII.

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126
Q

can statins be taken if pateint is trying to become pregnant?

A

Statins should be discontinued in women 3 months before conception due to the risk of congenital defects

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127
Q

what are the symptoms of Kearns- sayre syndrome?

A

Kearns-Sayre syndrome: onset in patients < 20 years old, external ophthalmoplegia, retinitis pigmentosa. Ptosis may be seen

can’t see ya syndrome

mitochondrial inheritance

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128
Q

what are the precipitants of pomphylax eczema/ dyshidrotic eczema?

A

high temperatures and humdity

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129
Q

what is the treatment for pomphylox?

A

cool compresses
emollients
topical steroids

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130
Q

what are the features of lateral medullary syndrome?

A

PICA stroke
cerebellar signs, contralateral sensory loss & ipsilateral Horner’s

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131
Q

what is the protocol for varicella exposure in preganancy?

A

<20 weeks and not immune:
VZIG as soon as possible

> 20 weeks and not immune:
VZIG or antivirals (aciclovir or valaciclovir) should be given days 7 to 14 after exposure

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132
Q

who gets VZ IG and who gets aciclovir?

A

To keep it simple:
administer VZIG to :
1. Pregnant women <20 weeks with exposure and no varicella antibodies
2. Newborn with peripartum exposure ( 7 days around birth)

Administer Acicloveir to:
1. Pregnant women who develop chickenpox
2. Pregnant women >20 weeks with exposure and no varicella antibodies
3.Immunocompromised who develop chickenpox
4. Immunocompromised with exposure to chockenpox

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133
Q

which genetic disorder is linked with high likelihood of crohns’ disease?

A

Turners syndrome is linked with crohn’s and autoimmune thyroiditis

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134
Q

what other markers other than ALP is diagnostic of Pagets’ disease?

A

procollagen type I N-terminal propeptide (PINP)
serum C-telopeptide (CTx)
urinary N-telopeptide (NTx)
urinary hydroxyproline

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135
Q

what is used for the management of venous ulceration?

A
  • compression bandaging
  • oral pentoxifylline - peripheral vasodilator
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136
Q

what are the features of endocervical cells?

A

koilocytes

  • enalrged nucleus
  • irregular nuclear membrane contour
  • nucleus stains darker than normal (hyperchormoasia)
  • perinuclear halo
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137
Q

what are the characteristic findings of hyposplenism on blood film?

A
  • target cells
  • howell-jolly bodies
  • pappenheimer bodies
  • siderotic granules
  • acanthocytes
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138
Q

what causes whipple’s disease?

A

Tropheryma whipplei - gram positive rod bacteria

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139
Q

what are the features of whipple’s disease?

A

abdominal pain, diarrhoea, steatorrhoea, migrating polyarthralgia, photosensitivity, skin hyperpigmentation, petechiae and peripheral oedema

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140
Q

how is whipple’s disease diagnosed?

A

It is diagnosed by demonstrating macrophages containing Periodic acid-Schiff (PAS) granules on jejunal biopsy

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141
Q

why is hyperpigmentation in whipple’s disease?

A

The hyperpigmentation is typically due to vitamin B3 malabsorption and subsequent deficiency.

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142
Q

what is the treatment for whipple’s disease?

A

Oral co-trimoxazole for a year is thought to have the lowest relapse rate, sometimes preceded by a course of IV penicillin

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143
Q

what is the treatement of Hypercalcaemia?

A

IV fluid resuscitation
IV bisphosphonates may be used
calcitonin - quicker effect than bisphosphonates

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144
Q

what are the features of tuberous sclerosis?

A
  • Depigmented ‘ash-leaf’ spots which fluoresce under UV light
  • Roughened patches of skin over lumbar spine (Shagreen patches)
  • Adenoma sebaceum (angiofibromas): butterfly distribution over nose
  • Fibromata beneath nails (subungual fibromata)
  • café-au-lait spots* may be seen
145
Q

what are the different differentials for causes of pneumonia?

A

Pneumonia + Alcoholic + Cavitation = Klebsiella
Pneumonia + Prior Flu = Staph Pneumonia
Pneumonia + Chicken Pox Rash = Varicella
Pneumoniae Pneumonia + Hemolytic Anemia = Mycoplasma
Pneumonia + Hyponatraemia + Travel History = Legionella
Pneumonia + Fleeting opacities = Cryptogenic Pneumonia
Pneumonia + Fits/LOC = Aspiration Pneumonia
Pneumonia + HSV oral lesion = Strep Pneumonia
Pneumonia + parrot = Chlamydia psitatssi
Pneumonia + farm animals = Q fever (coxillea brunetii)
Pneumonia + HIV = think pcp but if straight forward case strep pneumonia is still most common
Pneumonia + Cystic fibrosis = consider pseudomonas/Burkholderia
Pneumonia + COPD or exac = c1::Haemophilus Influenza
Commonest cause of CAP = Strep Pneumonia

146
Q

what is the cause of dengue fever?

A

dengue virus is a RNA virus of the genus flavivirus
transmitted by Aedes aegypti mosquito

147
Q

what are the features of dengue?

A

Retro-orbital headache, fever, facial flushing, rash, thrombocytopenia in returning traveller → ?dengue

myalgia, bone pain and arthralgia (‘break-bone fever’)
facial flushing - dengue

148
Q

what are the warning signs to look out for in dengue?

A

abdominal pain
hepatomegaly
persistent vomiting
clinical fluid accumulation (ascites, pleural effusion)

149
Q

what are the features of severe dengue (dengue haemorrhagic fever)?

A

Form of disseminated intravascular coagulation (DIC) resulting in:
- thrombocytopenia
- spontaneous bleeding

150
Q

what are the findings of limited cutaneous systemic scelorsis?

A
  • Raynaud’s may be the first sign
  • scleroderma affects face and distal limbs predominately
  • associated with anti-centromere antibodies

CREST - Calcinosis, Raynaud’s phenomenon, oEsophageal dysmotility, Sclerodactyly, Telangiectasia

151
Q

what are the features of diffuse cutaneous systemic sclerosis?

A

sceleroderma affects the trunk and proximal limb
Anti-scl 70 antibodies

most common cause of death - respiratory involvement - interstitial lung disease and pulmonary arterial hypertension

152
Q

what group of people do you need to be careful using zanamivir on?

A

asthmatics - may induce bronchospams

153
Q

what are the side-effects of sulfasalazine?

A
  • oligospermia
  • Stevens-Johnson syndrome
  • pneumonitis / lung fibrosis
  • myelosuppression, Heinz body anaemia, -
  • megaloblastic anaemia
  • may colour tears → stained contact lenses
154
Q

why does orbital cellulitis need IV antibiotics?

A

Patients with orbital cellulitis require admission to hospital for IV antibiotics due to the risk of cavernous sinus thrombosis and intracranial spread

155
Q

A 79-year-old woman is reviewed. She has taken bendroflumethiazide 2.5mg od for the past 10 years for hypertension. Her current blood pressure is 150/94 mmHg. Clinical examination is otherwise unremarkable. An echocardiogram from two months ago is reported as follows:

Ejection fraction 48%, moderate left ventricular hypertrophy. Minimal MR noted

what drug do you want to add?

A

echocardiogram shows a degree of left ventricular impairment. It is important an ACE inhibitor is started in such patients. This will help to both control her blood pressure and also slow the deterioration in her cardiac function.

156
Q

what are the adverse-effects of azathioprine?

A
  • bone marrow depression- consider a full blood count if infection/bleeding occurs
  • nausea/vomiting
  • pancreatitis
  • increased risk of non-melanoma skin cancer
157
Q

what is the diagnostic criteria for IBS?

A

A positive diagnosis of IBS should be made if the patient has abdominal pain relieved by defecation or associated with altered bowel frequency stool form,

in addition to 2 of the following 4 symptoms:

  1. altered stool passage (straining, urgency, incomplete evacuation)
  2. abdominal bloating (more common in women than men), distension, tension or hardness
    3.symptoms made worse by eating
  3. passage of mucus
158
Q

what are the features of ethylene glycol toxicity?

A

Divided into 3 stages:

Stage 1: symptoms similar to alcohol intoxication: confusion, slurred speech, dizziness

Stage 2: metabolic acidosis with high anion gap and high osmolar gap. Also tachycardia, hypertension

Stage 3: acute kidney injury

159
Q

what is the treatment for ethylene glycol toxicity?

A

fomepizole - inhibitor of alcohol dehydrogenase

160
Q

what are the conditions associated with angioid retina streaks?

A
  • pseudoxanthoma elasticum
  • ehler - danlos syndrome
  • paget’s disease
  • sickle cell anaemia
  • acromegaly
161
Q

what is the simple feature triad in churgs strauss / eosinophlic granulamatosis with polyangiitis?

A

Churg-Strauss syndrome as evidenced by the asthma, mononeuritis and eosinophilia

162
Q

who should recieve treatement for asymptomatic bacteruria?

A

Asymptomatic bacteriuria should not be treated except in pregnancy, children younger than 5 years or immunosuppressed patients due to the risk of complications

163
Q

what is the difference between lymphogranuloma venerum vs syphilis vs herpes simplex?

A

painful - HSV type 2, chancroid ( u/l painful inguinal l ) , Behcets

painless - syphilis, LGV ( painful inguinal l )

164
Q

what is the cause of cysticercosis?

A

Taenia solium - tapeworm
Often transmitted after eating undercooked pork

Treatment - bendazole

165
Q

why does phenytoin cause newborn develops widespread scalp and skin bruising 12 hours post-delivery?

A

Phenytoin induces vitamin K metabolism, which can cause a relative vitamin K deficiency, creating the potential for heamorrhagic disease of the newborn
Important for meLess important

166
Q

A 48-year-old Afro-Caribbean female is admitted with a fever and painful red eyes bilaterally. On examination, her temperature is 38.3ºC, heart rate 85bpm, respiratory rate 26/min, and oxygen saturation 93% on room air. Closer examination reveals bilateral swelling of her parotid glands.

A chest x-ray is performed, which reveals bilateral hilar lymphadenopathy. What is the most likely unifying diagnosis?

A

Heerfordt syndrome

Heerfordt’s syndrome (uveoparotid fever) there is parotid enlargement, fever and uveitis secondary to sarcoidosis

167
Q

what medication can be useful for drooling in parkinson’s disease?

A

Consider glycopyrronium bromide to manage drooling of saliva in people with Parkinson’s disease

168
Q

which factors increase the risk of cancer in UC?

A
  • Disease duration > 10 years
  • Patients with pancolitis
  • Onset before 15 years old
  • Unremitting disease
  • Poor compliance to treatment
169
Q

what does the blood test for paget’s disease look like?

A

Alkaline phosphatase is normally raised in Paget’s disease but blood tests such as calcium, phosphate, vitamin D and parathyroid hormone are usually unaffected

Other markers of bone turnover including hydroxyproline, which is raised in both the urine and serum, as well as procollagen type I N-terminal propeptide (PINP), C-telopeptide (CTx) and N-telopeptide (NTx).

170
Q

what is the difference in target INR between aortic and mitral metal valve replacement?

A

Mechanical valves - target INR:
aortic: 3.0
mitral: 3.5

171
Q

what are the surgical contraindications for non-small cell lung cancer resection?

A
  • stage IIIb or IV (i.e. metastases present)
  • FEV1 < 1.5 litres is considered a general cut-off point*
  • malignant pleural effusion
  • tumour near hilum
  • vocal cord paralysis
  • SVC obstruction
172
Q

what are the side-effects of phenytoin?

A

P- Pseudolymphoma, pancytopenia, P450 interaction
H-Hirsutism, Acne
E-Enlarged gums
N-Nystagmus-cerebellar syndrome
Y-Yellow browning of skin
T-teratogenic
O-Osteomalacia
I-Interference with folic acid absorption
Idiosyncracy
N-Neuropathies

173
Q

what are the side effects of valproate?

A

Vomiting
Alopecia
Liver toxicity
Pancreatitis/ Pancytopenia
Retention of fats (weight gain)
Oedema (peripheral oedema)
Anorexia
Tremor/teratogenicity
Enzyme inhibition

174
Q

what is the pathophysiology behind bullous pemphigoid?

A

secondary to the development of antibodies against hemidesmosomal proteins BP180 and BP230

175
Q

what is the unique feature of bullous pemphigoid?

A

there is stereotypically no mucosal involvement (i.e. the mouth is spared)

in reality around 10-50% of patients have a degree of mucosal involvement. It would, however, be unusual for an exam question to mention mucosal involvement as it is seen as a classic differentiating feature between pemphigoid and pemphigus.

176
Q

what is the mainstay of treatment for bullous pemphigoid?

A

oral corticosteroids

177
Q

if digoxin toxicity is suspected, when should the levels be measured

A

if toxicity is suspected, digoxin concentrations should be measured within 8 to 12 hours of the last dose

178
Q

what are the factors that precipitate digoxin toxicty?

A
  1. hypokalaemia - digoxin binds to the ATPase pump on the same site as potassium.
  2. increasing age
  3. renal failure
  4. mycocardial ischaemia
  5. hypomagnesaemia, hypercalcaemia, hypernatraemia, acidosis
    hypoalbuminaemia
    hypothermia
    hypothyroidism
179
Q

what is the pathophysiology behind pemphigus vulgaris?

A

antibodies directed against desmoglein 3, a cadherin-type epithelial cell adhesion molecule

180
Q

what is seen on biopsy of pemphigus vulgraris?

A

acantholysis on biopsy

181
Q

what are the different incubation periods for the different bugs that cause D&V?

A

Incubation period
1-6 hrs: Staphylococcus aureus, Bacillus cereus*
12-48 hrs: Salmonella, Escherichia coli
48-72 hrs: Shigella, Campylobacter
> 7 days: Giardiasis, Amoebiasis

*vomiting subtype, the diarrhoeal illness has an incubation period of 6-14 hours

182
Q

what is the simplistic presentation of Loeffler syndrome?

A

lofflers syndromme presents with fever, cough and night sweats (TB) like picture with transient patches on CXR in a person with history of travel to tropics. A Self limiting disease.

183
Q

what are the drug causes of gout?

A
  • diuretics - thiazides, furosemide
  • ciclosporin
  • alcohol
  • cytotoxic agents
  • pyrazinamide
  • aspirin -
184
Q

what do you need to be aware of when starting warfarin in patients with protein C deficiency?

A
  • skin necrosis following commencement fo warfarin

when warfarin is first started biosynthesis of protein C is reduced. This results in a temporary procoagulant state after initially starting warfarin, normally avoided by concurrent heparin administration. Thrombosis may occur in venules leading to skin necrosis

185
Q

what is the treatment for lambert eaton syndrome?

A
  1. treatment of underlying cancer
  2. immunosuppression, for example with prednisolone and/or azathioprine
  3. 3,4-diaminopyridine
  4. intravenous immunoglobulin therapy and plasma exchange may be beneficial
186
Q

what are the features of severe malaria?

A

schizonts on a blood film
parasitaemia > 2%
hypoglycaemia
acidosis
temperature > 39 °C
severe anaemia

187
Q

what are the complications of malaria?

A
  1. cerebral malaria: seizures, coma
  2. acute renal failure: blackwater fever, secondary to 3. intravascular haemolysis, mechanism unknown
  3. acute respiratory distress syndrome (ARDS)
  4. hypoglycaemia
  5. disseminated intravascular coagulation (DIC)
188
Q

what are the features of neonatal lupus erythematosus?

A
  • Leads to a condition termed neonatal lupus erythematosus
  • strongly associated withanti-Ro (SSA) antibodies
189
Q

what is the cause of erythrasma?

A

Generally asymptomatic, flat, slightly scaly, pink or brown rash usually found in the groin or axillae.

It is caused by an overgrowth of the diphtheroid Corynebacterium minutissimum

190
Q

what is seen under wood’s light for erythrasma?

A

coral red fluorscence

191
Q

what is the treatment for erythrasma?

A

topical miconazole or antibacterial

192
Q

how do you differentiate erythrasma and pityriasis versicolor?

A

Erythrasma : found in the groin or axillae, pruritis is rare , coral-red fluorescence color

Pityriasis versicolor : most commonly affects trunk ,mild Pruritis is common, pale yellow to white fluorescence color

193
Q

what are the common monoclonal antibodies, their targets and their use?

A

infliximab (anti-TNF): used in rheumatoid arthritis and Crohn’s

rituximab (anti-CD20): used in non-Hodgkin’s lymphoma and rheumatoid arthritis

cetuximab (epidermal growth factor receptor antagonist): used in metastatic colorectal cancer and head and neck cancer

trastuzumab (HER2/neu receptor antagonist): used in metastatic breast cancer

alemtuzumab (anti-CD52): used in chronic lymphocytic leukaemia

abciximab (glycoprotein IIb/IIIa receptor antagonist): prevention of ischaemic events in patients undergoing percutaneous coronary interventions

OKT3 (anti-CD3): used to prevent organ rejection

194
Q

what medications are contraindicated in HOCM?

A

ACE-inhibitors should be avoided in patients with HOCM.

Agents that reduce preload/afterload (such as nitrate, ACE inhibitors, nifedipine-type calcium antagonists) are contraindicated with HOCM due to possible aggravation of the outflow tract obstruction.

195
Q

what is the management of HOCM?

A

Amiodarone
Beta-blockers or verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis*

196
Q

what are the different translocation associated conditions?

A

t(9;22) is associated with chronic myeloid leukaemia

t(8;14) is associated with Burkitt lymphoma

t(11;14) is associated with mantle cell lymphoma

t(15;17) is associated with acute promyelocytic leukaemia

t(14:18) - Follicular lymphoma

197
Q

what are the conditions that cause hypokalemia with hypertension?

A

Liddle’s syndrome
Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism)
11-beta hydroxylase deficiency

198
Q

what is the values to denite impaired fasting glucose and OGTT 2-hr value?

A

> 7.0 mmol/l - impaired fasting glucose
OGTT - >11.1 mmol/l

199
Q

what is the treatment of restless leg syndrome?

A

dopamine agonists - ropinirole, pramipexole

200
Q

what medications are contraindicated in alzeimhers disease?

A

Donepezil can cause cardiac conduction issues, hallucination, dizziness.

Amitrip can cause cardiac conduction issues (long QT), dizziness, sedation.

Therefore the combination of the two is a recipe for disaster.

201
Q

what are the side-effects of tricyclic antidepressants?

A

Tri-CyCliCs: Convulsions, Coma, Cardiotoxicity (arrhythmia due to Na+ channel inhibition)

202
Q

what is the pathology of hereditary angioedema?

A

Associated with low plasma levels of the C1 inhibitor (C1-INH, C1 esterase inhibitor) protein.

C1-INH is a multifunctional serine protease inhibitor - the probable mechanism behind attacks is uncontrolled release of bradykinin resulting in oedema of tissues.

203
Q

what investigation shows hereditary angiooedema?

A

C1-INH level is low during an attack

low C2 and C4 levels are seen, even between attacks.

Serum C4 is the most reliable and widely used screening tool

204
Q

what is used in the treatment of herediatry angio-oedema?

A

IV C1 inhibitor concentrate , FFP

Does not respond to adrenaline, antihistamines or glucocorticoids

205
Q

what is used in the prophylaxis of hereditary angio-oedema?

A

anabolic steroid Danazol

206
Q

which endocarditis causative organism is associated with colon cancer?

A

Streptococcus bovis

the subtype Streptococcus gallolyticus is most linked with colorectal cancer

207
Q

what change in levothyroxine is required in pregnancy?

A

In pregnancy, anyone already on levothyroxine treatment should increase their dose.

Thyroid doses should be adjusted in steps of 25-50mcg.

In pregnancy, the increase in thyroid replacement is typically 20-50%, which normally equates to 25mcg-50mcg increase.

208
Q

where is the medial longitudinal fasciculus located in the brain?

A

The medial longitudinal fasciculus is located in the paramedian area of the midbrain and pons

209
Q

how do you differentiate TTP and HUS?

A

Both TTP and HUS as common symptoms of MAT,
MAT: M=Microangiopathi hemolytic anemia, A=Acute kidney injury T= Thrombocytopenia

Now, When there is MAT + Fever + Neurological signs = TTP
and MAT + bloody diarrhea = HUS

210
Q

what are the indications of urate lowering therapy in gout?

A

> = 2 attacks in 12 months
tophi
renal disease
uric acid renal stones
prophylaxis if on cytotoxics or diuretics

211
Q

when should urate lowering therapy be started?

A

it has traditionally been taught that urate-lowering therapy should not be started until 2 weeks after an acute attack, as starting too early may precipitate a further attack. The evidence base to support this however looks weak

212
Q

what are the contraindications for the use of metformin in the context of lactic acidosis?

A

metformin may cause lactic acidosis if taken during a period where there is tissue hypoxia. -recent myocardial infarction
- sepsis
- acute kidney injury
- severe dehydration

213
Q

what is the guidelines on treating benzodiazepine withdrawal?

A
  • switch patient to the equivalent dose of diazepam
  • reduce dose of diazepam every 2-3 weeks in steps of 2-2.5 mg
  • time needed for withdrawal can vary from 4 weeks to a year or more
214
Q

how is hyperthryoidism managed in pregnancy?

A

Propylthiouracil is used in the first trimester of pregnancy in place of carbimazole, as the latter drug may be associated with an increased risk of congenital abnormalities. At the beginning of the second trimester, the woman should be switched back to carbimazole

215
Q

what are the risk factors of squamous cell carcinoma?

A
  • Excessive exposure to sunlight / psoralen UVA therapy
  • Actinic keratoses and Bowen’s disease
  • Immunosuppression e.g. following renal transplant, HIV
  • smoking
  • long-standing leg ulcers (Marjolin’s ulcer)
  • genetic conditions e.g. xeroderma pigmentosum, oculocutaneous albinism
216
Q

what is the mechanism of action of dipyridamole?

A
  • inhibits phosphodiesterase, elevating platelet cAMP levels which in turn reduce intracellular calcium levels
  • other actions include reducing cellular uptake of adenosine and inhibition of thromboxane synthase
217
Q

what causes hyperthyroidism in pregnancy?

A

Increase in the levels of thyroxine-binding globulin (TBG).
This causes an increase in the levels of total thyroxine but does not affect the free thyroxine level.

218
Q

what causes hyperthyroidism in pregnancy?

A

Increase in the levels of thyroxine-binding globulin (TBG).
This causes an increase in the levels of total thyroxine but does not affect the free thyroxine level.

219
Q

what are the causes of hypertrichosis?

A

drugs: minoxidil, ciclosporin, diazoxide
congenital hypertrichosis lanuginosa, congenital hypertrichosis terminalis
porphyria cutanea tarda
anorexia nervosa

220
Q

what condition is pheochromocytoma associated with?

A

Phaeochromocytoma is associated with 1,2,3
NF-1, MEN 2, VHL (chromosome 3)

221
Q

what medications should be avoided in lewy body dementia?

A

neuroleptics should be avoided in Lewy body dementia as patients are extremely sensitive and may develop irreversible parkinsonism. Questions may give a history of a patient who has deteriorated following the introduction of an antipsychotic agent

222
Q

what is the pathology behind paroxysmal nocturnal haemoglobinuria?

A

An acquired disorder leading to haemolysis (mainly intravascular) of haematological cells.

It is thought to be caused by increased sensitivity of cell membranes to complement due to a lack of glycoprotein glycosyl-phosphatidylinositol

GPI can be thought of as an anchor which attaches surface proteins to the cell membrane

complement-regulating surface proteins, e.g. decay-accelerating factor (DAF), are not properly bound to the cell membrane due a lack of GPI

thrombosis is thought to be caused by a lack of CD59 on platelet membranes predisposing to platelet aggregation

223
Q

what is the diagnostic test for paroxysmal noctural haemoglobinura?

A

Flow cytometry of blood to detect low levels of CD59 and CD55

224
Q

what drugs cause urticaria

A

aspirin
penicillins
NSAIDs
opiates

225
Q

what is the treatment for paroxysmal nocturnal haemoglobinuria?

A
  • blood product replacement
  • anticoagulation
  • eculizumab, a monoclonal antibody directed against terminal protein C5, is currently being trialled and is showing promise in reducing intravascular haemolysis
  • stem cell transplantation
226
Q

what is the mainstay of treatement for crytosporidium diarrhoea?

A

supportive therapy

227
Q

what are the tyeps of hereditary sensorimotor neuropathy?

A

HSMN type 1 : demyelinating pathology
HSMN type 2 : axonal pathology

228
Q

what is the defect in Herediatry sensory motor neuropathy type 1? charcot-marie tooth disaese

A

defect in PMP-22 gene (encodes for myelin)
motor symptoms predominate

distal muscle wasting, pes cavus, clawed toes
foot drop, leg weakness often first features

229
Q

what complements are low in SLE?

A

C1q, C1rs, C2, C4 deficiency

predisposes to immune complex disease

230
Q

what is DRESS syndrome?

A

drug reaction with eosinophilia and systemic symptoms

morbilliform skin rash - 80% of cases - exfoliative dermatitis, high fever and inflammation
Vesicles and bullae
Erythroderma
mucosal involvement
facial swelling

231
Q

what medications cause DRESS syndrome?

A

Allopurinol,
Anti-epileptics
Antibiotics
Immunosuppresants
HIV treatment
NSAIDS

232
Q

which medications are considered safe during preganancy to treat rheumatoid arthritis?

A

sulfasalazine and hydroxychloroquine are considered safe in pregnancy

233
Q

what is the pathology of homocystinuria?

A

A rare autosomal recessive disease caused by a deficiency of cystathionine beta synthase.

This results in severe elevations in plasma and urine homocysteine concentrations.

234
Q

what are the investigations necessary to diagnose homocystinuria?

A
  1. increased homocysteine levels in serum and urine
  2. cyanide-nitroprusside test: also positive in cystinuria
235
Q

what are the typical features of homocytsinuria?

A
  • have fine, fair hair
  • MSK - marfoanoid features, osteoporosis, kyphosis
  • neurological - learning difficulities, seizures
  • ocular - downward dislocation of the lens, severe myopia
  • increased risk of arterial and venous thromboembolism
236
Q

what is the treatment for homocystinuria?

A

B6 - pyridoxine

237
Q

how do you differentiate the cause of horner syndrome?

A

head, arm, trunk = central lesion: stroke, syringomyelia
just face = pre-ganglionic lesion: Pancoast’s, cervical rib
absent = post-ganglionic lesion: carotid artery

238
Q

what is the treatment of organophosphate poisoning?

A

Atropine

239
Q

what is the test for systemic mastocystosis?

A
  • urinary histamine
  • raised serum tryptase levels
240
Q

how do you differentiate systemic mastocytosis from carcinoid syndrome?

A

Abdo pain, flushing and diarrhoea may be similar

however, the urticaria pigmentosa - Darier’s sign is unique to systemic mastocystosis

241
Q

what conditions is pesudogout associated with?

A

haemochromatosis
hyperparathyroidism
low magnesium, low phosphate
acromegaly, Wilson’s disease

242
Q

what is the most common cause of peritonitis in periotoneal dialysis?

A
  • coagulse-negative staphylococci - staph. epidermidis
243
Q

what is the treatment for peritonitis secondary to peritoneal dialysis?

A

the BNF recommends vancomycin (or teicoplanin) + ceftazidime added to dialysis fluid OR vancomycin added to dialysis fluid + ciprofloxacin by mouth

aminoglycosides are sometimes used to cover the Gram negative organisms instead of ceftazidime

244
Q

what bundle branch blocks do congenital heart disease cause?

A

OS primum- LBBB= when in Primary school, you are LEFT alone by your parents

OS secundum- RBBB= when in Secondary school, you take the RIGHT path to success

245
Q

what is the treatment for cryptosporium infection in the immunocompromised?

A

nitazoxanide may be used for immunocompromised patients

rifaximin is also sometimes used for immunocompromised patients/patients with severe disease

246
Q

What are the drugs associated with raised prolactin?

A
  • metoclopramide, domperidone
  • phenothiazines
  • haloperidol
    very rare: SSRIs, opioids
247
Q

what is the transformation seen in polycythaemia vera?

A

Polycythaemia rubra vera - around 5-15% progress to myelofibrosis or AML

248
Q

what are the drugs causing lung fibrosis?

A
  1. MTX
  2. Ethambutol
  3. ergot-DA agonists eg bromocriptine, cabergoline, pergolide
  4. Sulfasalazine
  5. Bleomycin/Busulphan
  6. Amiodarone
  7. Nitrofurantoin
249
Q

what are the exceptions to the inheritance pattern rule?

A

Autosomal recessive conditions are ‘metabolic’ - exceptions: inherited ataxias

Autosomal dominant conditions are ‘structural’ - exceptions: Gilbert’s, hyperlipidaemia type II

250
Q

what are the side-effects of cisplatin?

A

HOP

Hypomagnesaemia
Ototoxicity
peripheral neuropathy

251
Q

what are all the most common X-ray findings? (to split)

A

1- pseudogout: chondrocalcinosis

2- gout: larg punched out erosions in x-ray (tophi), double contour sign on US

3- Psoriatic arthritis:
Erosive changes and new bone formation
Periostitis
Pencil in cup appearances

4- Ankylosing spondylitis:
Syndismocytes formation
Subchondoral erosions
Sclerosis
Squiring of vertebra
Romanus leasion
Bamboo spine

5- Rheumatoid arthritis:
Soft tissue swelling
Subchondoral osteoporosis
Joint space narrowing
Subluxation and Ankylosis

6- Osteoarthritis:
Joint space narrowing
Osteophytes
Subchondoral cyst

7- Paget’s disease:
Lytic and sclerotic lesions on skul e.g.

8- Rickets:
Winding of wrist joint
Cupping, fraying and ……
Widening of epiphysis

9- osteopetrosis:
Bone on bone lesions

10- Osteomalacia:
Translucent bands (looser’s zones or pseudofracture)

252
Q

what are the features of Digeroge syndrome?

A

CATCH22:
C - Cardiac abnormalities
A - Abnormal facies
T - Thymic aplasia
C - Cleft palate
H - Hypocalcaemia/ hypoparathyroidism
22 - Caused by chromosome 22 deletion

253
Q

what is the immune problem seen in di-george syndrome?

A

T-cell deficiency and dysfunction.

at risk of viral and fungal infections
parathyroid gland hypoplasia → hypocalcaemic tetany
thymus hypoplasia
T-lymphocyte deficiency/dysfunction

254
Q

what are the features suggestive of diphtheria?

A

severe tonsillitis, neck swelling (lymphadenopathy - bull’s neck)

Sequelae include myocarditis and rhythm abnormalities (in particular heart block)

255
Q

what is the treatment for post-cholescystectomy syndrome?

A

Management is often difficult, but often involves a low-fat diet and the introduction of bile acid sequestrants, such as Cholestyramine, to bind the excess bile acids and thus preventing lower gastrointestinal signs.

256
Q

what are the causes of renal papillary necrosis?

A

POSTCARDS:
pyelonephritis,
obstruction of the urogenital tract
sickle cell disease
tuberculosis,
cirrhosis of the liver
analgesia/alcohol abuse,
renal vein thrombosis
diabetes mellitus,
systemic vasculitis.

257
Q

when is buproprion contraindicated?

A

CI in epilepsy, pregnancy and breast feeding

258
Q

what are the causes of high anion gap metabolic acidosis?

A

CAT MUDPILES

C- carbon monoxide, cyanide, CHD
A - Aminoglycosides
T - Theophylline

M- methanol
U- Uraemia
D - Dibetic, alcohol and starvation ketoacidosis
P - paracetamol,
I - Iron, isoniazid, inborn errors of metabolism
L - lactic acidosis
E - ethanol, ethlene glycol
S - salicylate

259
Q

what are the different types of cryoglobulinaemia?

A

Type I (25%):
monoclonal - IgG or IgM
associations: multiple myeloma, Waldenstrom macroglobulinaemia

Type II (25%)
mixed monoclonal and polyclonal: usually with rheumatoid factor
associations: hepatitis C, rheumatoid arthritis, Sjogren’s, lymphoma

Type III (50%)
polyclonal: usually with rheumatoid factor
associations: rheumatoid arthritis, Sjogren’s

260
Q

what are the risk factors for allopurinol induced severe cutaneous reaction?

A

HLA-B*5801 allele testing is the most appropriate next step in management.

risk factors include diuretic use, ethnicity (Thai descent), and chronic kidney disease

261
Q

why is chloroquine substituted with primaquine after acute malaria episode in non-falciparum malaria?

A

Primaquine is used in non-falciparum malaria to destroy liver hypnozoites and prevent relapse

262
Q

what is the side effects of NRTI such as zidovudine?

A

peripheral neuropathy

263
Q

what is seen on liver biopsy of autoimmune hepatitis~?

A

inflammation extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis

264
Q

what are the causes of upper zone lung fibrosis?

A

C - Coal worker’s pneumoconiosis
H - Histiocytosis/ hypersensitivity pneumonitis
A - Ankylosing spondylitis
R - Radiation
T - Tuberculosis
S - Silicosis/sarcoidosis

265
Q

what are the causes of lower zone lung fibrosis

A

idiopathic pulmonary fibrosis
most connective tissue disorders (except ankylosing spondylitis) e.g. SLE
drug-induced: amiodarone, bleomycin, methotrexate
asbestosis

‘RAID’- rheumatological conditions, asbestos exposure, idiopathic and drug-induced.

266
Q

what is lesch-nyhan syndrome?

A

hypoxanthine-guanine phosphoribosyl transferase (HGPRTase) deficiency

x-linked recessive therefore only seen in boys

features: gout, renal failure, neurological deficits, learning difficulties, self-mutilation

267
Q

what is the pathophysiology in hepatorenal syndrome?

A

vasoactive mediators cause splanchnic vasodilation which in turn reduces the systemic vascular resistance. This results in ‘underfilling’ of the kidneys. This is sensed by the juxtaglomerular apparatus which then activates the renin-angiotensin-aldosterone system, causing renal vasoconstriction which is not enough to counterbalance the effects of the splanchnic vasodilation

268
Q

what is diagnostic of SBP?

A
  • paracentesis: neutrophil count > 250 cells/ul
  • the most common organism found on ascitic fluid culture is E. coli
269
Q

what is the mx of SBP?

A

IV cefotaxime

270
Q

when is abx prophylaxis suggested for SBP?

A
  • patients who have had an episode of SBP
  • patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome
  • NICE recommend: ‘Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less until the ascites has resolved’
271
Q

what sx in lymphoma represent a poor prognosis?

A

‘B’ symptoms also imply a poor prognosis
weight loss > 10% in last 6 months
fever > 38ºC
night sweats

272
Q

what is the diagnostic criteria for ARDS?

A
  • acute onset (within 1 week of a known risk factor)
  • pulmonary oedema: bilateral infiltrates on chest x-ray (‘not fully explained by effusions, lobar/lung collapse or nodules)
  • non-cardiogenic (pulmonary artery wedge pressure needed if doubt)
  • pO2/FiO2 < 40kPa (300 mmHg)
273
Q

How do you differentiate pseudogout from gout on x-ray

A

Calcification of the triangular fibrocartilage suggests chondrocalcinosis

274
Q

Who do you offer LTOT to?

A

Anyone with pO2 < 7.3kPa

pO2 7.3-8kPA:
- secondary polycythemia
- peripheral oedema
- pulmonary hypertension

275
Q

what is the tx for sleep paralysis?

A

if troublesome clonazepam may be used

276
Q

what are the causes of erythema nodosum?

A

NODOSUM
NO: NO causes in 80% of cases
D : Drugs (sulfonamides; amoxicillin)
O : Oral contraceptive pills
S : Sarcoidosis/ Tuberculosis
U : Ulcerative colitis; Crohn’s disease; Behcet disease
M: Micro
Viral : HSV; EBV; Hep B; Hep C
Bacterial: campylobacter; salmonella; streptococci; Brucellosis
Parasite : Amoebiasis; Giardiasis

277
Q

why is there increased need for thyroid hormones in pregnancy?

A

In pregnancy, there is an increase in thyroid-binding globulin (TBG), an increase in urinary iodine excretion and deiodinase activity of the placenta which increase thyroid hormone metabolism.

278
Q

what are the features of mcardles disease?

A
  • muscle pain and stiffness following exercise
  • muscle cramps
  • myoglobinuria
  • low lactate levels during exercise
279
Q

what are the cut offs for bariatric surgery?

A

with risk factors (T2DM, BP etc): > 35 kg/m^2
no risk factors: > 40 kg/m^2

280
Q

which type of leishmaniasis causes different types of presentation?

A

Tropica = Topical

Braziliensis = Buccal

Dono-V-ani = Visceral

281
Q

what is Heyde syndrome?

A

aortic stenosis and angiodysplasia resulting in chronic gastrointestinal blood loss

282
Q

watery diarrheoa and use of PPI in young pt. ddx?

A

microscopic collitis

283
Q

what are the features of behcet’s syndrome?

A

The classic triad of symptoms are oral ulcers, genital ulcers and anterior uveitis

284
Q

what are the layers of epidermis called?

A

Corneum
Lucidum
Granulosum
Spinosum
Basale (germinativum)

come lets get sun burnt

285
Q

what is Liddle syndorme?

A

Liddle’s syndrome is a rare autosomal dominant condition that causes hypertension and hypokalaemic alkalosis. It is thought to be caused by disordered sodium channels in the distal tubules leading to increased reabsorption of sodium.

Treatment is with either amiloride or triamterene

286
Q

what are GNs associated with low complement levels?

A

post-streptococcal glomerulonephritis
subacute bacterial endocarditis
systemic lupus erythematosus
mesangiocapillary glomerulonephritis

287
Q

what are the indications of NIV?

A
  1. COPD with respiratory acidosis pH 7.25-7.35 - the BTS guidelines state that NIV can be used in patients who are more acidotic (i.e. pH < 7.25) but that a greater degree of monitoring is required (e.g. HDU) and a lower threshold for intubation and ventilation should be used
  2. type II respiratory failure secondary to chest wall deformity, neuromuscular disease or obstructive sleep apnoea
  3. cardiogenic pulmonary oedema unresponsive to CPAP
  4. weaning from tracheal intubation
288
Q

why is plasmodium knowlesi infections particualrly dangerous?

A

P. knowlesi has the shortest erythrocytic replication cycle, leading to high parasite counts in short periods of time

289
Q

what causes retroperitonela fibrosis

A

Riedel’s thyroiditis
previous radiotherapy
sarcoidosis
inflammatory abdominal aortic aneurysm
drugs: methysergide

290
Q

how do you differentiate black water fever and schistosomiasis?

A

Blackwater fever is a rare complication of malaria which can be fatal. It is caused by large intravascular haemolysis resulting in haemoglobinuria, anaemia, jaundice and acute kidney injury. Urine is classically black or dark red in colour.The cause of the massive haemolysis is unknown. The treatment is with antimalarials, intravenous fluids and in some cases dialysis. Urinalysis reveals blood which is not seen on microscopy as it is haemoglobinuria.

Schistosomiasis has an acute onset which includes symptoms of fever, chills, headache and fatigue but symptoms of haematuria do not come till the chronic phase as a result of bladder fibrosis and calcification, this presents more insidiously. In addition, in schistosomiasis, urine microscopy would show red cell casts.

291
Q

what is tx of latent TB?

A

The treatment for latent tuberculosis is 3 months of isoniazid (with pyridoxine) and rifampicin OR 6 months of isoniazid (with pyridoxine)

292
Q

what are the absolute CI for chest drain insertion?

A

INR > 1.3
Platelet count < 75
Pulmonary bullae
Pleural adhesions

293
Q

causes of drug induced lupus?

A

procainamide
hydralazine

isoniazid
minocycline
phenytoin

SHIMP
Sulphonamides
Hydralazine (renal involvement)
Isoniazid
Phenytoin, Penicillin, Procainamide

294
Q

what is the tx for methaemoglobinaemia?

A

NADH methaemoglobinaemia reductase deficiency: ascorbic acid
IV methylthioninium chloride (methylene blue) if acquired

295
Q

what is peutz-jegher syndrome?

A

Peutz-Jeghers syndrome is an autosomal dominant condition characterised by numerous hamartomatous polyps in the gastrointestinal tract

pigmented lesions on lips, oral mucosa, face, palms and soles

296
Q

what are signs of worsening pancreatitis?

A

age > 55 years
hypocalcaemia
hyperglycaemia
hypoxia
neutrophilia
elevated LDH and AST

297
Q

what is the tx for brucellosis?

A

doxycycline and streptomycin

298
Q

how do you diff brucellosis from other infective causes?

A

sacroiliitis - spinal tenderness

complications - osetomyelitis, infective endocarditis, orchitis

299
Q

which of the drugs can be cleared on haemodialysis?

A

BLAST

Barbiturate
Lithium
Alcohol (inc methanol, ethylene glycol)
Salicylates
Theophyllines (charcoal haemoperfusion is preferable)

300
Q

typical presentation of Autoimmune hepatitis?

A

acute hepatitis: fever, jaundice

amenorrhoea
ANA/SMA/LKM1 antibodies, raised IgG levels

301
Q

what is seen on liver biopsy of autoimmune hep?

A

liver biopsy: inflammation extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis

302
Q

what is the cause of melioidosis?

A

Burkholderia pseudomallei

distributed environmental saprophyte in soil and fresh surface water in endemic regions

303
Q

what are risk factors of melioidosis?

A

Diabetes mellitus (the strongest risk factor)
Chronic renal, liver, or lung disease (e.g., cystic fibrosis)
Immunocompromised states (e.g., malignancy, long-term glucocorticoid use)
Occupational exposure: agricultural work

304
Q

what is the tx of melioidosis?

A

Initial intensive therapy: IV ceftazidime, imipenem, or meropenem for 10–14 days

eradication therapy: oral TMP/SMX (plus doxycycline) for 3–6 months

305
Q

what is the tx for leprosy?

A

rifampicin, dapsone and clofazimine

306
Q

what ablation can cure Atrial Flutter?

A

radiofrequency ablation of the tricuspid valve isthmus

307
Q

what abx is given for liver abscess?

A

amoxicillin + ciprofloxacin + metronidazole

308
Q

what are the different HIV drugs used?

A

Nucleoside analogue reverse transcriptase inhibitors (NRTI) - tenofivir, abacavir , ‘ines’ - zidovudine…

Non-nucleoside reverse transcriptase inhibitors - NNRTI - nevirapine, efavirenz

Protease inhibitors - virs

integrase inhibitors - raltegravir, elvitegravir, dolutegravir

309
Q

fever, sweats, rigors , spleenomegaly with pancytopaenia. recent travel to sudan. skin is dark and ashen. whats the dx?

A

Visceral leishmaniasis

Leishmania donovani

grey skin - ‘kala-azar’ means black sickness
pancytopaenia secondary to hypersplenism
the gold standard for diagnosis is bone marrow or splenic aspirate

Textbooks

Links
DermNet NZ71
Leishmaniasis review

Royal College of Physicians42
2011 Leishmaniasis review
Report broken link
Media
YouTube
What is Leishmaniasis? An introduction and overview
Let’s Learn About Bugs - YouTube97

310
Q

What are the indications of chest drain insertion in pleural effusion?

A
  1. Patients with frankly purulent or turbid/cloudy pleural fluid on sampling should receive prompt pleural space chest tube drainage.
  2. The presence of organisms identified by Gram stain and/or culture from a non-purulent pleural fluid sample indicates that pleural infection is established and should lead to prompt chest tube drainage.
  3. Pleural fluid pH < 7.2 in patients with suspected pleural infection indicates a need for chest tube drainage
311
Q

typical blood picture of tumour lysis syndrome?

A

uric acid > 475umol/l or 25% increase
potassium > 6 mmol/l or 25% increase
phosphate > 1.125mmol/l or 25% increase
calcium < 1.75mmol/l or 25% decrease

312
Q

tx for peritonitis secondary to peritoneal dialysis

A

vancomycin (or teicoplanin) + ceftazidime added to dialysis fluid OR vancomycin added to dialysis fluid + ciprofloxacin by mouth

313
Q

poor prognostic markers of ALL

A

FAB L3 type
T or B cell surface markers
Philadelphia translocation, t(9;22)
age < 2 years or > 10 years
male sex
CNS involvement
high initial WBC (e.g. > 100 * 109/l)
non-Caucasian

314
Q

Evolocumab mechanism?

A

PCSK9-mediated LDL receptor degradation.

315
Q

different types of immunodeficiencies

A

B cell disorders of 1o immunodeficiency = ‘Sh*tty B Cells’
1. Selective IgA deficiency
2. Brutons
3. CVID

Combined B&T cell disorders = ‘WASH your Bs and Ts’
1. Wiskott-Aldrich syndrome
2. Ataxic Telangiectasia
3. SCID
4. Hyper IgG syndromes

T cell disorder = Di George

316
Q

skin disorders associated with malignancy

A

1 - Black patches (AN)- Gastric CA
2 - Woody and hot red skin (AI and dermatomyositis) - Lymphoma
3 - Hairy skin (AHL) - Lung and ovary CA
4 - complex design/pattern skin (EGR) - Lung CA
5 - Multiple VTE (MT) - Pancreatic CA
6 - Gangrene and sweet syndrome (PG) - Haem malignancies
7 - Hard dark yellow skin (Tylosis) - Esophegeal CA
8 - Generalised/migratory erythema (NME) - Glucagonoma

317
Q

how do you differentiate microscopic colitis from crohns or uC?

A

The lack of abdominal pain, rectal bleeding or extra-intestinal manifestations make a diagnosis of ulcerative colitis or Crohn’s disease less likely.

. The history of proton-pump inhibitor use associated with the development of watery diarrhoea, suggests microscopic colitis.

318
Q

how do you differntiate MALT lymphoma from anaplastic thyroid cancer?

A

Anaplastic thyroid cancer is rare (1-2% of thyroid cancers). - can cause compression symptoms

Mucosa-associated lymphoid tissue (MALT) lymphoma is correct. Although this is a rare form of thyroid lymphoma it is associated with a previous history of Hashimoto’s thyroiditis and histology shows extranodal marginal B-cells.

319
Q

what is PTH levels like in hyperparathyroidism?

A

high or normal

320
Q

what is the tx for hyperthyroidism in preganancy

A

1st trimester - propylthiouracil

2nd trimester - carbimazole

321
Q

what is AION?

A

seen in Giant cell arteritis

occlusion of the posterior ciliary artery (a branch of the ophthalmic artery) → ischaemia of the optic nerve head. Fundoscopy typically shows a swollen pale disc and blurred margins

322
Q

how do you differntaite AML from Acute promyelocyctic leukaemia?

A

classically disseminated intravascular coagulation

+
AML blood picture

323
Q

what is the tx for hemiballism?

A

Antidopaminergic agents (e.g. Haloperidol) are the mainstay of treatment

324
Q

what test is used for HIV screening of asymptomatic individuals?

A

Combined HIV antibody/antigen tests are now the first-line test for HIV screening of asymptomatic individuals or patients with signs and symptoms of chronic infection

325
Q

how long does it take to develop HIV antibodies?

A

most people develop antibodies to HIV at 4-6 weeks but 99% do by 3 months

326
Q

differentiate CADSIL vs MELAS?

A

CADASIL = migraine + multiple strokes
MELAS = lactic acidosis + multiple strokes

mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS)

327
Q

what is mode of action of duloxetine?

A

Serotonin and noradrenaline reuptake inhibitors

328
Q

what is early x-ray feature of rheumatoid?

A

joint space and juxta-articular osteopaenia.

329
Q

differnentiate between TB vs cryptococcal meningitis in HIV pts?

A

lymphocytic CSF with high protein and low glucose in this case could be due to both cryptococcal and TB meningitis, however the insidious onset of symptoms, very high protein and low glucose compared to the plasma glucose (<1/3 of plasma) points more towards TB meningitis. Also this man has a relatively high CD4 count (240) and only a mildly raised opening pressure which makes cryptococcal meningitis more unlikely. TB and HIV co-infection are common, especially in sub-Saharan Africa and should always be considered.

330
Q

what is the tx for discoid lupus erthematosus?

A

topical steroid cream
oral antimalarials may be used second-line e.g. hydroxychloroquine

331
Q

what is the notable adverse effect of ticagrelor?

A

dyspnoea - due to the impaired clearance of adenosine

332
Q

when is ticagrelor contraindicated?

A

Ticagrelor is contraindicated in patients with a:

  1. high risk of bleeding, those with a history of intracranial haemorrhage,
  2. and those with severe hepatic dysfunction.

It is also to be used with caution in those with acute asthma or COPD, as ticagrelor-treated patients experience higher rates of dyspnoea.

333
Q

why is CKMB better than troponin in recurrent MIs?

A

Creatine kinase (CK-MB) remains elevated for 3 to 4 days following infarction. Troponin remains elevated for 10 days. This makes CK-MB useful for detecting re-infarction in the window of 4 to 10 days after the initial insult

334
Q

what are the diffs for black eschars?

A

Anthrax or Rickettsia

335
Q

classical tumour lysis blood picture

A

hyperkalaemia
hyperphosphataemia
hypocalcaemia
hyperuricaemia
acute renal failure

336
Q

what are the features of familial mediterranean fever? also known as recurrent polyserositis

A

pyrexia
abdominal pain (due to peritonitis)
pleurisy
pericarditis
arthritis
erysipeloid rash on lower limbs

337
Q

what tx is used after methotrexate in rheumatoid arthritis?

A

ustekinumab (targets both IL-12 and IL-23) and secukinumab (targets IL-17)

apremilast: phosphodiesterase type-4 (PDE4) inhibitor → suppression of pro-inflammatory mediator synthesis and promotion of anti-inflammatory mediators

338
Q

what are the three cardinal clinical manifestations of leprosy?

A

hypopigmented skin lesions
nerve thickening
peripheral nerve palsies

339
Q

how do you differentiate lepromatous leprosy from tuberculoid leprosy

A

Low degree of cell mediated immunity → lepromatous leprosy (‘multibacillary’)
extensive skin involvement
symmetrical nerve involvement

High degree of cell mediated immunity → tuberculoid leprosy (‘paucibacillary’)
limited skin disease
asymmetric nerve involvement → hypesthesia
hair loss

340
Q

what is the tx for leprosy?

A

rifampicin, dapsone and clofazimine

341
Q

what is the tx for leprospiromatosis?

A

high-dose benzylpenicillin or doxycycline

342
Q

what is the tx for brucellosis?

A

doxycycline and streptomycin

343
Q

what is the tx for SBP?

A

intravenous cefotaxime

344
Q

what is the tx for alzheimers disease?

A

1st line - anti acetylcholinesterase - donepezil, galantaine or rivastigmine

2nd line - memantine (NMDA antagonist)

345
Q

what is the tx for amoebiasis?

A
  • oral metronidazole
  • lumnial agent - diloxanide furoate
346
Q

culture negative causes of endocarditis?

A

prior antibiotic therapy
Coxiella burnetii
Bartonella
Brucella
HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella

347
Q

what is the tx for anthrax?

A

ciprofloxacin

348
Q

causes of osteoporosis?

A
  • Steroids
  • Hyperthyroidism, hyperparathyroidism, hypercalciuria
  • Alcohol and tobacco
  • Thin (BMI < 18.5)
  • Testosterone deficiency
  • Early menopause
  • Renal or liver failure
  • Erosive/inflammatory diseases (e.g. myeloma, RA)
  • Dietary Ca deficiency/malabsorption, DM type 1
349
Q

what are the indications to start steorids in sarcoidosis?

A

PUNCH

Parenchymal lung involvement
Uveitis
Neuro involvement
Cardio involvement
Hypercalcaemia

350
Q

how does sarcoidosis cause hypercalcaemia?

A

Sarcoidosis mainly causes hypercalcaemia through forming increased concentrations of calcitriol, the active component of vitamin D. This is as a result of increased activity of 1α hydroxylase produced by the sarcoid macrophages.

351
Q

what are ECG features of hypothermia?

A

Hypothermia features: Jesus, Its Bloody Freezing

J wave
Irregular pattern (long QT interval, atrial and ventricular arrhythmias)
Bradycardia
First degree and higher heart blocks

352
Q

what is the tx of thyrotoxic storm?

A
  1. beta blocker - IV propanolol
  2. anti-thyroid drugs - methimazole or propylthiouracil
  3. Lugol’s iodine
  4. dexamethasone - blocks conversion of T4 - T3
353
Q

difference between holmes adie and Argyll Robertson pupils?

A

Argyll Robertson pupils
are bilateral small pupils that reduce in size on a near object (i.e., they accommodate), but do not constrict when exposed to bright light (i.e., they do not react to light). (ARP=accommodation reflex present), in DM, syphilis

Holmes-Adie syndrome, is a rare neurological disorder affecting the pupil of the eye. In most patients the pupil is larger than normal (dilated) Absent or poor tendon reflexes

354
Q

what are the drugs that exacerbate myasthenia gravis?

A

P3 LGBtQ

P3–Procainamide/penicillamine/phenytoin
L -lithium
G- gentamicin
B- beta blockers
Q - quinidine

355
Q

what are the features of plummer-vinson syndrome?

A

iron deficiency anaemia, dysphagia due to esophageal webs, and atrophic glossitis

356
Q

live attenuated vaccines?

A

BCG
MMR
oral polio
yellow fever
oral typhoid

357
Q

steven john syndorme drugs?

A

penicillin
sulphonamides
lamotrigine, carbamazepine, phenytoin
allopurinol
NSAIDs
oral contraceptive pill

358
Q

what is AA amyloidosis?

A

AA amyloid

A for precursor serum amyloid A protein, an acute phase reactant

seen in chronic infection/inflammation
e.g. TB, bronchiectasis, rheumatoid arthritis

features: renal involvement most common feature

MRCP p1 (13 decks)

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