Things I keep forgetting Flashcards
Acanthrosis nigricans assx
Gastric Ca
Acquired icthyosis assx
Lymphoma
Acquired hypertrichosis lanuginosa assx
GI + lung Ca
Dermatomyositis assx
ovarian + lung ca
erythema gyratum repens assx
lung ca
erythroderma assx
lymphoma
migratory thrombophlebitis assx
pancreatic ca
necrolytic migratory erythema assx
glucagonoma
pyoderma gangrenosum assx
myeloproliferative disorders
IBD
Rheumatoid arthritis
PBC
Chronic active hepatitis
sweet’s syndrome assx
haem malignancy
tylosis assx
oesophageal ca
Lymphoma skin manifestations
acquired ichthyosis, erythroderma
Lung ca skin manifestations
acquired hypertrichosis lanuginosa
dermatomyositis
erythema gyratum repens
Vibagatrin key SE
visual field defects - needs monitoring
Minimal change GN biopsy findings
normal glomeruli on light microscopy
electron microscopy shows fusion of podocytes and effacement of foot processes
Prognosis in minimal change GN
1/3 have just one episode
1/3 have infrequent relapses
1/3 have frequent relapses which stop before adulthood
Which pO2s do RBCs sickle at for HbAS?
2.5-4 kPa
Which pO2s do RBCs sickle at for HbSS?
5-6 kPa
Positively skewed and negatively skewed distributions: mean, median, mode
Normal (Gaussian) distributions: mean = median = mode
Positively skewed distribution: mean > median > mode
Negatively skewed distribution mean < median < mode
think positive going forward with ‘>’, whilst negative going backwards ‘<’
Causes of warm AIHA
idiopathic
autoimmune (SLE)
neoplasia (lymphoma, CLL)
drugs (methyldopa)
causes of cold AIHA
neoplasia (lymphoma)
infections (mycoplasma, EBV)
Likelihood ratio for a +ve test
sensitivity/(1-specificity)
Likelihood ratio for a -ve test
(1-sensitivity)/specificity
Heberden’s nodes
Osteoarthritis - painless DIPJ swelling
Osteoarthritis common joints and symptoms
CMCs, DIPJs, usually bilateral
Heberden’s, Bouchard’s nodes
Squaring of thumbs - CMC deformity –> fixed thumb adduction
Provoked by movement, relieved by rest
Stiffness worsened with ina ctivity
Bouchard’s nodes
Osteoarthritis - PIPJ swelling
Coarctation of aorta murmur
Late systolic
From which primaries are lung mets more commonly calcified?
Chondrosaracoma
Osteosarcoma
What primaries cause cannonball lung mets?
Renal cell ca
Choriosarcoma
Prostate Ca
What primaries cause haemorrhagic pulmonary mets?
Choriosarcoma
Angiosarcoma
What primaries cause miliary pattern of lung mets?
Renal cell ca
Malignant melanoma
What primary causes cavitating lung mets?
Squamous cell ca
What is the regime of choice when starting insulin in T1DM?
Twice daily insulin detemir
When do you start metformin in T1DM?
If BMI>25 - consider it
Causes of membranous GN
Idiopathic (anti phospholipase A2 Abs)
Infections: HBV, malaria, syphilis
Malignancy (5-20%): prostate, lung, lymphoma, leukaemia
Drugs: gold, penicillamine, NSAIDs
Autoimmune: SLE (class V), thyroiditis, rheumatoid
Prognosis in membranous GN
one-third: spontaneous remission
one-third: remain proteinuric
one-third: develop ESRF
Membranous GN Rx
ACE inhibitors/ARBs
Severe/progressive - immunosuppression:
Steroids + cyclophosphamide
Rituximab if moderate risk of progression
Anticoagulate for high-risk
Good prognosis factors in membranous GN
Female
Young age at presentation
Asymptomatic proteinuria of modest degree at presentation
Discoid lupus Rx
- topical steroids
- oral antimalarials eg hydroxychloroquine
Drug-induced lupus Abs
ANA 100%
Anti-histone 80-90%
anti-Ro
anti-Smith
-ve for dsDNA
Occupational asthma chemicals assx:
Isocyanates (most common - spray painting, foam moulding using adhesives)
Platinum salts
Soldering flux resin
Glutaraldehyde
Flour
Epoxy resins
Proteolytic enzymes
HHS criteria:
hypovolaemia
hyperglycaemia >30
hyperosmolality >320
no ketonaemia/acidosis
IL-1 source
macrophages
IL-1 function
acute inflammation
Induces fever
Il-2 source
Th1 cells
IL-2 functions
stimulates growth + differentiation of T cell response
IL-3 source
activated T helper cells
IL-3 functions
Stimulates differentiation + proliferation of myeloid progenitor cells
IL-4 source
Th2 cells
IL-4 functions
Stimulates proliferation + differentiation of B cells
IL-5 source
Th2 cells
IL-5 function
eosinophil production stimulation
IL-6 source
macrophages
Th2 cells
Il-6 functions
Stimulates B cell differentiation
Fever
IL-8 source
Macrophages
IL-8 function
neutrophil chemotaxis
IL-10 source
Th2 cells
IL-10 function
Inhibits Th1 cytokine production
(Known as human cytokine synthesis inhibitory factor - anti-inflammatory)
IL-12 source
dendritic cells
macrophages
B cells
IL-12 function
Activates NK cells, stimulates differentiation of naive T cells into Th1 cells
TNF alpha source
macrophages
TNF alpha functions
Fever
Neutrophil chemotaxis
IFN gamma source
Th1 cells
IFN gamma function
activates macrophages
Which cytokines do macrophages produce?
(Alpha 1268)
IL-1, 6, 8, 12
TNF alpha
Which cytokines do Th1 cells produce?
Th 1- 2,3 gamma
IL-2, 3
IFN gamma
Which cytokines do Th2 cells produce?
IL-4, 5, 6, 10, 13
CURB 65
Confusion (AMTS 8 or less)
Urea>7
RR>30
BP<90/60
Age >65
Enhanced liver fibrosis test composition
Hyaluronic acid + procollagen III + tissue inhibitor of metalloproteinase 1
Conditions causing increased KCO with normal or reduced TLCO
Pneumonectomy/lobectomy
Scoliosis/kyphosis
Neuromuscular weakness
Ankylosis of costovertebral joints (eg Ank Spond)
Causes of SAAG>11g/L
Portal HTN
Liver disorders: cirrhosis, ALD, acute liver failure, liver mets
Cardiac: right heart failure, constrictive pericarditis
Budd-chiari
PVT
Veno-occlusive disease
Myxoedema
Causes of SAAG<11g/L
hypoalbuminaemia: nephrotic syndrome, severe malnutrition
Malignancy: peritoneal carcinomatosis
Infections: tuberculous peritonitis
Others: pancreatitis, bowel obstruction, biliary ascites, postoperative lymphatic leak, serositis
What factors increase iron absorption
Vitamin C
Gastric acid
What reduces iron absorption
PPIs
Tetracyclines
Gastric achlorhydria
Tannin (in tea)
Pemphigus vulgaris antibodies
vs desmoglein 3 (a cadherin-type epithelial cell adhesion molecule)
Pemphigus vulgaris Sx
Flaccid blisters - easily ruptured vesicles + bullae
Mucosal ulceration common (oral 50-70%)
Nikolsky’s sign +ve (spread of bullae following horizontal, tangential pressure to skin)
Bullous pemphigoid Abs
Vs hemidesmosomal proteins BP180, BP230 in basement membrane
Bullous pemphigoid sx
Tense blisters - heal without scarring, usually around flexures
No mucosal involvement
Bullous pemphigoid biopsy
Immunfluorescence: IgG and C3 at dermoepidermal junction
Pemphigus vulgaris biopsy
acantholysis
Function of Th1 cells
Involved in cell-mediated response and delayed type 4 hypersensitivity
Function of Th2 dcells
mediating humoral (Ab) immunity
Azoles MOA
inhibits 14 alpha demethylase –> reduces ergosterol production from lanosterol –> reduces plasma membrane structural integrity/stability
Azoles SE
CYP450 Inhibitor
Hepatotoxic
Terbinafine MOA
Inhibits squalene epoxidase –> ultimately reduces ergosterol production –> reduces plasma membrane structural integrity/stability
Terbinafine SE
Pancytopenia
Agranulocytosis
Hepatotoxic
Echinocandins (Gaspofungin/any -fungins) MOA:
Beta-glucan synthase inhibition –> prevents beta glucan transport to cell wall to be used for its formation
Echinocandin SE
flushing
Amphotericin B MOA
binds to ergosterol forming transmembrane channel –> tears in walls (amphoTEARicin) –> leads to monovalent ion (K, Na, H, Cl) leakage + cell death
Amphotericin B SE
nephrotoxic, flu-like sx, hypoK, HypoMg, hepatotoxic, phlebitis
Nystatin MOA:
binds to ergosterol forming transmembranechannel –> makes little holes –> monovalent ion leakage + cell death
Griseofulvin MOA
interacts with microtubules, disrupts mitotic spindle
Griseofulvin SE
CYP450 inducer
teratogenic
Flucytosine MOA
converted by cytosine deaminase to 5-fluorouracil, inhibits thymidylate synthase –> attacks DNA –> disrupts fungal protein synthesis
FLucytosine SE
vomiting
Aciclovir MOA
guanosine analogue, inhibits viral DNA polymerase
Aciclovir SE
crystalline nephropathy - crystalluria
Ganciclovir MOA
guanosine analogue, inhibitis DNA polymerase
Ganciclovir SE:
myelosuppression/agranulocytosis
Foscarnet MOA
pyrophosphate analogue, inhibits DNA polymerase
Foscarnet SE
nephrotoxicity, hypoCa, hypoMg, seizures
Ribavirin MOA
guanosine analogue, inhibits IMP dehydrogenase, interferes with mRNA capping
Ribavirin SE
haemolytic anaemia
Amantadine MOA
inhibits M2 protein, uncoating of virus, releases dopamine from nerve endings
Amantadine SE
confusion, ataxia, slurred speech
Oseltamivir MOA
neuraminidase inhibitor
Cidofovir MOA
acyclic nucleoside phosphonate, independent of phosphorylation by viral enzymes
Cidofovir SE
nephrotoxicity
What is the aim of post-marketing observational studies for new drugs, following clinical trials?
To study profile of adverse effects (esp in pts not studied during clinical trials, such as those with liver, renal disease, pregnant, children)
Phases of clinical trials
Phase 0: exploratory, assess drug behaviour in human body, assesses pharmacokinetics, pharmacodynamics
Phase I: side-effects, healthy volunteers
Phase IIa: optimal dosing.
Phase IIb: efficacy
Phase III: effectiveness, 100-1000s of people, RCTs
Phase IV: postmarketing surveillance, long-term SE, effectiveness
A 79-year-old woman was admitted for elective hip-replacement surgery.
On examination, she was pale. There was 2-cm splenomegaly and there were small discrete axillary lymph nodes.
Investigations:
haemoglobin 107 g/L (115–165)
white cell count 34.5 × 109/L (4.0–11.0)
platelet count 183 × 109/L (150–400)
What is the most likely diagnosis?
CLL
Livedo reticularis causes
HIP CASE
Homocystinuria
Idiopathic (most common)
PAN
Cryoglobulinaemia
Antiphospholipid syndrome
SLE
EDS
A 37-year-old woman presented with a history of intermittent lightheadedness.
Examination was normal.
Investigations:
ECG normal
24-hour ambulatory ECG tracing
atrial and ventricular premature beats; nocturnal bradycardia and Mobitz type I atrioventricular block, and supraventricular tachycardia
Which abnormality on the 24-hour ambulatory ECG is clinically most important?
SVT
Wilson’s disease - where does the copper often deposit in the brain?
basal ganglia, esp putamen, globus pallidus
Wilson’s syndrome serum and urinary findings
Reduced serum caeruloplasmin
Reduced TOTAL serum copper
But increased FREE serum copper
Increased 24hr urinary copper excretion
Wilson’s genetics
Aut Rec
Chr 13
ATP7B gene defect
Argyll Robertson pupils
ARP
Accommodation Reflex Present but
Pupillary Reflex Absent
Often bilateral, small, irregular pupils
Causes: Neurosyphilis, DM
Holmes-Adie Pupils
Unilateral, dilated pupil.
Once constricted, remains so for abnormally long time, slow reaction to accommodation
Holmes Adie syndrom= HA pupil + absent ankle/knee reflexes
Prevention of calcum stones
Lifestyle: high fluid intake, add lemon juice to drinking water, avoid carbonated drinks, limit salt intake
Drugs:
Potassium citrate - reduces urinary supersaturation of ca salts by forming soluble complexes with ca ions and inhibits crystal growth and aggregation. Useful for recurrent stones
Thiazides if very high Ca in urine
Genotypes in A1AT
PiMM - normal
PiMZ - heterozygous carrier
PiSS - 50% have normal A1AT levels
PiZZ - 10% have normal A1AT levels. Severe phenotype
Hypercholesterolaemia causes
Nephrotic syndrome
Cholestasis
Hypothyroidism
Hypertriglyceridaemia causes
DM
Obesity
CKD
Thiazides
Non-selective beta blockers
Unopposed oestrogen
Liver disease
ETOH
Thyroid cancers from commonest to least common
Papillary
Follicular
Medullary
Anaplastic
Lymphoma
A 77-year-old man presented with increasing pains around his lower back and lower limb girdle. He had recently presented with symptoms of hesitancy and post-micturition dribbling.
Investigations:
ESR 28 mm/1st h (<20)
serum adjusted calcium 2.34 mmol/L (2.20–2.60)
serum phosphate 0.80 mmol/L (0.80–1.45)
serum alkaline phosphatase 2985 U/L (45–105)
serum prostate-specific antigen 6 μg/L (<4.0)
What is the most likely cause of this man’s pain?
Paget’s
A 50-year-old man presented with a 2-day history of multiple painful joints. Two weeks previously, he had been started on treatment with allopurinol for tophaceous gout. His only other medication was paracetamol. He had a history of excess alcohol intake.
On examination, his temperature was 37.5°C and there was acute inflammation of the finger joints, wrists, knees and ankles.
Investigations:
serum gamma glutamyl transferase 90 U/L (<50)
serum CRP 180 mg/L (<10)
serum urate 0.65 mmol/L (0.23–0.46)
What is the most likely cause of his symptoms?
Allopurinol therapy triggering acute flare of gout
Due to falling serum urate levels –> uric acid crystals detaching from articular cartilage
Burkitt’s lymphoma genetics
Overexpression of c-Myc
t(8:14)
t(8:14) brings c-Myc gene under control of immunoglobulin heavy chain promoter and renders it constitutively active
Mantle cell lymphoma genetics
t(11:14)
Deregulation of cyclin D1 (BCL-1) gene
Follicular lymphoma genetics
t(14:18)
Increased BCL-2 transcription
Optimal time for vaccination when splenectomy is planned?
1 month pre-surgery
Infection prophylaxis in splenectomy
HiB + Men A&C + annual flu + pneumococcal every 5 yrs + lifelong penicillin V
Types of Hodgkin’s disease (commonest to rarest)
Nodular sclerosing
Mixed cellularity
Lymphocyte predominant
Lymphocyte depleted
Poor prognosis factors for Hodgkin’s
Age>45
Male
Stage IV
Hb<105
Lymphocyte<600
WCC>15000
Albumin <40
A 17-year-old girl presented with a single, painless, enlarged cervical lymph node. She was asymptomatic.
Investigations:
chest X-ray enlarged mediastinal lymph nodes
What is the most likely diagnosis?
Hodgkin’s
In severe haemoptysis requiring treatment, where does bleeding originate from?
Bronchial arteries (90%)
Pulmonary arteries (5%)
Causes of acute interstitial nephritis
Drugs (25%): penicillin, rifampicin, NSAIDs, allopurinol, furosemide
Systemic: SLE, sarcoidosis, Sjogren’s
Infection: Hantavirus, staph
Features of acute interstitial nephritis
fever
rash
arthralgia
eosinophilia
mild renal impairment
HTN
Sterile pyuria
white cell casts
Papillary necrosis causes
POSTCARDS
Pyelonephritis
Obstructive uropathy
Sickle cell
TB
cirrhosis
analgesia/alcohol
renal vein thrombosis
DM
systemic vasculitis
Papillary necrosis sx
fever, loin pain, haematuria
‘cup and spill’ - papillary necrosis with renal scarring on biopsy
Lichen planus
violaceous, flat-topped papules, which are often seen on the flexor surfaces of the wrists, lower back and ankles as well as elsewhere on the skin
can Koebnerise (lesions arise at area of skin that has been traumatised), resulting in linear pattern from scratching
Lacy white pattern on buccal mucosa (Wickham’s striae)
Can cause non-scarring alopecia if on scalps
GI complication of systemic sclerosis
Malabsorption due to SIBO in sclerosed small intestine
40% of patients
Causes of foot drop
Common peroneal nerve lesion
L5 radiculopathy
Sciatic nerve lesion
Superficial/deep peroneal nerve lesion
CN lesions
Common peroneal nerve lesion sx
Foot drop
Weakness: foot dorsiflexion, eversion, extensor hallucis longus
Sensory loss: over dorsum of foot + lower lateral part of leg
Wasting: anterior tibial and peroneal muscles
A 47-year-old woman was being treated with lithium for bipolar affective disorder.
On examination, her BP was 168/104 mmHg.
What is the most appropriate antihypertensive drug for her?
Amlodipine
Not ACE inhibitor because of renal risk in light of lithium
What antibody mediates hyperacute rejection?
IgG
Headache, increasing drowsiness, focal neuro sx + seizures in a woman shortly post partum
Dx?
Venous sinus thrombosis
Miller Fisher syndrome features
Internal and external ophthalmoplegia
Areflexia
Ataxia
Descending paralysis
GBS variant
Miller Fisher Abs
GQ1b
A 58-year-old man with congestive heart failure remained oedematous despite treatment with furosemide 120 mg daily.
Investigations:
serum sodium 134 mmol/L (137–144)
serum potassium 3.4 mmol/L (3.5–4.9)
serum urea 10.6 mmol/L (2.5–7.0)
serum creatinine 156 µmol/L (60–110)
What other finding is most likely?
Options:
high plasma aldosterone concentration
high serum cortisol concentration
low plasma angiotensin II concentration
low plasma atrial natriuretic peptide concentration
low plasma renin concentration
high plasma aldosterone concentration
Pathophysiological activation of RAAS due to reduced renal perfusion pressure in CCF
Acromegaly investigations
IGF-1 levels first - not diagostic
To diagnose, need OGTT (GH suppressed in normal, but no suppression in acromegaly)
Post-exposure prophylaxis of HIV
3 drug ART for 1 month
A 21-year-old woman, who was undergoing chemotherapy for non-Hodgkin lymphoma, presented 2 days after being in contact with her nephew, for 2 hours, on the day that he developed a chickenpox rash.
Investigations:
varicella serology negative
What is the most appropriate management?
Give varicella zoster immunoglobulin as she is immunocompromised
Diarrhoea within 1 week of travel
E Coli commonest (ETEC)
A 36-year-old HIV-positive man presented with a 1-week history of generalised pruritus. He had had unprotected anal sex 2 months previously while on holiday in Spain. He had previously been vaccinated against hepatitis B virus, with an adequate antibody response.
On examination, his temperature was 37.8°C and he was jaundiced. Examination was otherwise normal.
Investigations:
serum total bilirubin 99 µmol/L (1–22)
serum aspartate aminotransferase 754 U/L (1–31)
serum alkaline phosphatase 173 U/L (45–105)
CD4 count 550 × 106/L (430–1690)
anti-hepatitis A IgM antibody negative
What is the most likely diagnosis?
Options:
acute hepatitis C
acute hepatitis D
CMV infection
syphilis
toxoplasmosis
Acute Hep C
Parietal lobe lesion features
Receptive dysphasia, dyslexia, inattention, sensory inattention, apraxia, astereognosis (tactile agnosia), inferior homonymous quadrantanopia
Gerstmann syndrome (if dominant parietal angular gyrus lesion) –> alexia, acalculia, finger agnosia, agraphia, left-right limb disorientation
A 58-year-old man was seen with progressive breathlessness in the outpatient clinic. He had undergone coronary artery bypass grafting 3 years previously and this had been complicated by a resternotomy for tamponade. He recovered well but had started to feel breathless and fatigued over the past 12 months. He had a history of type 2 diabetes mellitus and hypertension. He was a current smoker.
A diagnosis of constrictive pericarditis was made.
What is the most common physical finding seen in this group of patients?
Options:
ascites
finger clubbing
hepatomegaly
pericardial knock
pleural effusion
Hepatomegaly - the earliest and most consistent feature of pericardial constriction of the options here.
Ascites (a later phenomenon than hepatomegaly) and pericardial knock (recognised in around 50% of cases) are also features of pericardial constriction, making this a true “best-of” question. Finger clubbing is not a feature of constriction, however, and pleural effusion is uncommon.
Features of constrictive pericarditis
SOB
Right heart failure features: elevated JVP, ascites, oedema, hepatomegaly
Prominent X and Y descent
Pericardial knock (loud S3)
Kussmaul’s sign
Common cause of myocardial infarction in relation to pregnancy
Coronary artery dissection
How to diagnose PBC
AMA M2 subtype diagnostic 98%
Other Ix:
Raised IgM
USS/MRCP - to exclude other causes of extrahepatic obstruction
C7 dermatomes
Middle Finger and palm of hand
C6 dermatomes
Thumb and index finger
T4 dermatomes
nipples
T4 at the teatpore
T10 dermatomes
Umbilicus
L4 dermatome
Knee caps
Down on aLL 4s
L5 dermatome
big toe, dorsum of foot
S1 dermatome
Lateral foot, small toe
S1 is the smallest one
Triceps reflex nerve roots
C7, 8
Biceps reflex nerve roots
C5, 6
Ankle jerk reflex nerve roots
S1, 2
Knee jerk reflex nerve roots
L3, 4
Which skin layer does lipodermatosclerosis affect?
Hypodermis
If extensive, papillary dermis
Waterlow score parameters
Body weight/BMI
Nutritional status
Continence
Skin type
Mobility
Age
Sex
Erythrodermic psoriasis Rx
topical white soft paraffin smeared all over skin
A 24-year-old woman presented with shortness of breath of sudden onset. She had been at a nightclub and had been drinking wine but denied taking any illicit substances. She had no relevant medical history. She was a non-smoker.
On examination, her temperature was 37.0°C, her pulse was 100 beats/min and her BP was 110/70 mmHg. Her respiratory rate was 32 breaths/min and her oxygen saturation was 98% (94–98) breathing air.
Investigations:
arterial blood gases, breathing air:
PO2 12.9 kPa (11.3–12.6)
PCO2 3.8 kPa (4.7–6.0)
pH 7.44 (7.35–7.45)
H+ 36 nmol/L (35–45)
bicarbonate 19 mmol/L (21–29)
base excess –2.0 mmol/L (±2.0)
chest X-ray normal
What is the most likely diagnosis?
Hyperventilation
Superior mesenteric artery supply
Small intestine from distal duodenum to 2/3 of transverse colon
H pylori strongest association with GI issues
Duodenal ulcers
Lesser degree - gastric ulcers and carcinoma
Pulsus alternans
severe LVF due to cardiomyopathy, CAD, systemic HTN, AS
Pulsus bisferiens
Mod-severe AR
Combined AS + AR
RF for completed suicide
male
Older age
Efforts to avoid discovery
Planning
Leaving written note
Final acts
Violent method
Social isolation
Isosorbide mononitrate MOA
nitric oxide donor –> stimulation of guanylate cyclase –> cGMP production –> vasodilation
Posterior STEMI ECG
dominant R wave in V1-3 with ST depression
Posterior cardiac supply
Posterior descending artery
From RCA in 85% of people (right dominant)
From LCx in 15% (left dominant)
A 42-year-old woman presented complaining of “worms” in the skin of her arms and legs for the past 9 months. She could feel the worms moving, and had tried to get them out of her skin using a needle. She reported that the worms were gradually spreading and she was afraid they would lead to her death.
On examination, she was anxious. There were multiple needle marks on the skin of her arms and legs. Examination was otherwise normal.
What is the most likely diagnosis?
Options:
delusional disorder
depressive psychosis
factitious disorder
generalised anxiety disorder
somatic symptom disorder
Delusional disorder - delusional parasitosis
A 67-year-old woman presented with palpitations and a goitre. Propranolol was started to improve her symptoms.
On examination, she had a coarse tremor and sweaty palms, but no thyroid eye signs.
Investigations:
serum thyroid-stimulating hormone <0.03 mU/L (0.4–5.0)
serum free T4 25.0 pmol/L (10.0–22.0)
technetium-99m scan of thyroid increased uptake in right upper lobe, with uptake suppressed in rest of thyroid gland
What is the most appropriate treatment for her thyroid condition?
Answers:
carbimazole
prednisolone
propylthiouracil
radioiodine
total thyroidectomy
Radioiodine - to treat toxic adenoma - an autonomous nodule causing hyperthyroidism
How to calculate osmolality
(2xNa) + (2xK) + glucose + urea
Ivabradine MOA
inhibits funny channels
Ivabradine criteria
LVEF<35% + sinus rhythm + rate >75bpm (contraix for lower resting rates as blocks cahnnel responsible for cardiac pacing)
Hydralazine MOA
elevates cGMP, smooth muscle relaxation in arterioles
CHF Rx
- ACE inhibitors + beta blockers
- Spiro/eplerenone + SGLT-2 inhibitors
- Ivabradine, sacubitril-valsartan, digoxin, hydralazine + Nitrates or CRT
Offer annual flu vaccine + one-off pneumococcal vaccine (every 5 yrs if splenic dysfunction or CKD)
Blood donation contraix
Cancers
Heart conditions
If you received blood products after 1980
HIV +ve
Organ transplant recipient
HBV, HCV +ve
Injected non-prescription drugs
Hemibalism lesion
Basal ganglia’s subthalamic nucleus
Internuclear ophthalmoplegia lesion
medial longitudinal fasciculus
Located in paramedian area of midbrain and pons
Where does haloperidol have central anti-emetic action?
D2 antagonism centrally at the area postrema - a medullary structure controlling vomiting
A 72-year-old man presented with loss of the lower half of the visual field of his right eye, with no associated pain. He had type 2 diabetes mellitus and was being treated for hypertension.
Examination showed normal visual acuity in both eyes, with an inferior altitudinal field defect in his right eye. Fundoscopy of his left eye was normal, and the upper part of the right optic disc showed mild disc swelling. No fundal haemorrhages were seen. His BP was 160/90 mmHg.
What is the most likely diagnosis?
Options:
optic neuritis
panuveitis
posterior communicating artery aneurysm
retinal artery occlusion
retinal vein thrombosis
Retinal artery occlusion
Visual field deffect makes this more likely
Branch retinal vein thrombosis assx with fundal haemorrhages (not seen here)
Optic neuritis, panuveitis leads to visual acuity impairment + pain
Posterior communicating artery aneurysm typically presents with 3rd nerve palsy with dilation
Which muscle is involved with torticollis
contracture of the ipsilateral sternocleidomastoid muscle which leads to the chin being pushed to the opposite side.
An 85-year-old woman presented with breathlessness that had developed over the previous 2 years. She complained of a cough that frequently woke her from sleep. She had been treated with radiotherapy for a cervical lymphoma 20 years previously.
On examination, she was thin, but had no abnormal physical signs. Her oxygen saturation was 95% (94–98) breathing air.
Investigations:
high-resolution CT scan of chest basal fibrosis associated with dilated bronchi, but no honeycombing or ground-glass change
What is the most likely diagnosis?
Answers:
bronchiectasis
chronic aspiration
idiopathic pulmonary fibrosis
radiation pneumonitis
sarcoidosis
Chronic aspiration
The symptoms described are consistent with chronic aspiration occurring in the elderly. The CT findings are radiological bronchiectasis, a sequela of recurrent episodes of aspiration pneumonia. This does not, however, equate to a clinical diagnosis of bronchiectasis. The absence of honeycombing and ground-glass opacities counts against the diagnosis of radiation pneumonitis and idiopathic pulmonary fibrosis.
Erythema nodosum causes
Infections: Strep, TB, Brucellosis, Yersinia
Systemic: sarcoidosis, IBD, Behcet’s
Malignancy/lymphoma
Drugs: penicillins, sulphonamides, COCPs, pregnancy
A 23-year-old man was admitted with a 3-day history of lower cramping abdominal pain and fever. He had mild diarrhoea, but no blood in his stool. He had not travelled recently.
On examination, he was tender in his right iliac fossa. There were raised, tender, red nodules on his shins.
Investigations:
CT scan of abdomen cluster of lymph nodes at appendix suggestive of mesenteric adenitis
What is the most likely cause of his symptoms?
Answers:
Campylobacter jejuni infection
Salmonella enteritidis infection
tuberculosis
ulcerative colitis
Yersinia enterocolitica infection
Yersinia enterocolitica infection
The history of a non-specific diarrhoeal disease with right iliac fossa pain would most commonly be due to campylobacter. However, the finding of a “cluster of lymph nodes at appendix suggestive of mesenteric adenitis” points more to yersinia infection, which can mimic Crohn’s disease and appendicitis (pseudoappendicitis).
PNH features
Triad: Intravasc haemolytic anaemia, pancytopenia, venous thrombosis (Budd-Chiari)
Haemoglobinuria in morning
Aplastic anaemia in some
A 78-year-old man presented with a 3-month history of haematuria, increasing tiredness and breathlessness on exertion.
On examination, he looked pale.
Investigations:
haemoglobin 78 g/L (130–180)
MCV 108 fL (80–96)
white cell count 2.6 × 109/L (4.0–11.0)
neutrophil count 0.9 × 109/L (1.5–7.0)
platelet count 78 × 109/L (150–400)
blood film nucleated red blood cells, myelocytes and metamyelocytes
What is the most likely cause of his abnormal blood film?
Answers:
aplastic anaemia
bone marrow metastases
hypothyroidism
myelodysplasia
vitamin B12 deficiency
Bone marrow metastases
Pancytopenia with leukoerythroblastic film suggestive of bone marrow infiltration
Aplastic anaemia and hypothyroidism generally are associated with a normal blood film, MDS with abnormal blood cell appearances (e.g. poikilocytosis) and vitamin B12 deficiency with the characteristic hypersegmented neutrophils. A further clue in the stem is the haematuria, which indicates an underlying pathology.
A 26-year-old woman with a previous history of deep venous thrombosis was treated with low-molecular-weight heparin for a further episode proven by a Doppler ultrasound scan. She also reported that she had had two first-trimester spontaneous miscarriages. She was currently using contraception.
Investigations:
prothrombin time 13.0 s (11.5–15.5)
activated partial thromboplastin time 50 s (30–40)
anticardiolipin IgG antibodies 62 U/mL (<10)
pregnancy test negative
What is the most appropriate treatment?
Answers:
apixaban
aspirin
dabigatran
low-molecular-weight heparin
warfarin
LMWH
APLS here - should go for warfarin but it can’t be used so LMWH should be used at this time
Anti phospholipid syndrome antibodies
anti-beta 2 glycoprotein I
Lupus anticoagulant
Anticardiolipin
APLS Rx
primary thromboprophylaxis with low dose aspirin
Secondary thromboprophylaxis with lifelong warfarin (INR 2-3)
Recurrent thromboembolic: warfarin (INR 3-4) + low dose aspirin
Digoxin half-life
36 hrs
Term used to describe an abnormal number of chromosomes but not abnormal numbers of complete chromosome sets
aneuploid
Cavernous sinus CN lesions
III, IV, V1, VI
Hydatid disease Rx
Albendazole
Cysticercosis Rx
niclosamide
How to distinguish between irritant vs allergic contact dermatitis
No vesicles, only erythema: irritant
Vesicles, weeping eczema: allergic
Causes of hypokalaemia with alkalosis
Vomiting
Thiazides, loop diuretics
Cushing’s
Conn’s
Liddle’s
ALL Good prognosis
FAB L1 type
Common ALL
Pre-B phenotype
Low initial WBC
deletion (9p)
Hyperdiploidy
ALL poor prognosis
FAB L3 type
T or B cell markers present
t(9;22) (Philadelphia translocation)
age <2 yrs or >10yrs
Male sex
CNS involvement
high initial WBC (>100)
non-Caucasian
Huntington’s genetics
Aut Dom CAG trinucleotide repeat
Pseudohypoparathyroidism Dx
Measuring urinary cAMP and PO4 after PTH infusion
Increased cAMP and PO4 in hypoPTH, but no change in type 1 pseudohypoPTH
In type II psuedohypoPTH cAMP rises, PO4 does not rise
Features of psuedohypoPTH
low IQ, short stature, shortened 4th, 5th metacarpals
low Ca, high PO4, high PTH
Tetanus 1st line abx
IV metronidazole
Botulism vs Tetanus
Botulism causes flaccid paralysis vs spastic paralysis in tetanus
Botulism toxin blocks ACh release, Tetanus toxin prevents release of inhibitory GABA at NMJ
When to refer to nephrology for proteinuria
ACR >70
ACR >30 + persistent haematuria (after UTI excluded)
ACR 3-29 + persistent haematuria + RFs (eg declining eGFR, CVS disease)
Cyclophosphamide
alkylating agent, causes DNA crosslinking
Inhibitory effect on B cells, CD4+ T cells, CD8 + T cells
SE: haemorrhagic cystitis, myelosuppression, TCC
Bleomycin
Degrades preformed DNA
SE: lung fibrosis
Anthracyclin
Stabilises DNA topoisomerase II complex, inhibits DNA, RNA synthesis
SE: CDM
Methotrexate
inhibits dihydrofolate reductase and thymidylate synthesis
SE: myelosuppression, mucositis, liver fibrosis, lung fibrosis
Fluorouracil
Pyrimidine analogue, blocks thymidylate synthase (during S phase), induces cell cycle arrest + apoptosis
SE: myelosuppression, mucositis, dermatitis
6-mercaptopurine
Purine analogue activated by HGPRTase, reduces purine synthesis
SE: myelosuppression
Cytarabine
Pyrimidine antagonist. Interferes with DNA synthesis, esp during S-phase of cell cycle, inhibits DNA polymerase
SE: myelosuppression, ataxia
Vincristine, vinblastine
Inhibits microtubule formation
Vincristine SE: reversible peripheral neuropathy, paralytic ileus
Vinblastine SE: myelosuppression
Docetaxel
Prevents microtubule depolymerisation & Disassembly, decreases free tubulin
SE: neutropenia
Irinotecan
Inhibits topoisomerase I, preventing supercoiled DNA relaxation
SE: myelosuppression
Cisplatin
Causes DNA crosslinking
SE: ototoxicity, peripheral neuropathy, hypoMg
Hydroxyurea/hydroxycarbamide
Inhibits ribonucleotide reductase, decreases DNA synthesis
SE: myelosuppression
Which cardiac enzyme is the 1st to rise
Myoglobin
Which cardiac enzyme is the last to rise?
LDH
Which cardiac enzyme is best to look for reinfarction?
CK-MB (returns to noral after 2-3 days whilst trop-T stays elevated for 7-10 days)
Tuberous Sclerosis features
HAMARTOMAS
Hamartoma (retinal)
Adenoma sebaceum (angiofibromas)
Mental retardation
Ash leaf spots
Rhabdomyoma
Tubers
Optic haemartomas
Mitral regurgitation
Astrocytomas, Angiomyolipomata (renal)
Seizures, Shagreen patches
+cafe au lait spots, polycystic kidneys, subungual fibromata,
Can see cafe au lait spots
NF1 features
Cafe au lait spots
peripheral neurofibromas
Lisch nodules (iris hamartomas)
Scoliosis
Phaeochromocytoma
NF2 features
Schwannomas - bilateral vestibular, mutliple intracranial
Meningiomas
Ependymomas
Von Hippel-Lindau syndrome genetics
Aut dom VHL mutation in Chr 3
(3 letters in VHL)
Von Hippel Lindau Syndrome features
VHLS
Vitreous Haemorrhages
Haemangiomas (cerebellar + retinal)
Lots of cysts
Sadly, cancers (renal clear cell + endolymphatic sac)
Phaeochromocytomas
Foster-Kennedy syndrome
Frontal lobe tumour causing ipsilateral optic atrophy + contralateral papilloedema
Sulphsalazine SE:
rashes
oligospermia
Heinz body anaemia
megaloblastic anaemia
lung fibrosis
GI upset
Headache
Agranulocytosis
Pancreatitis
Interstitial nephritis
Subacute (De Quervain’s) thyroiditis thyroid scintigraphy findings
Globally reduced uptake of iodine-131
Friedrich’s ataxia genetics
Aut rec
GAA repeat in X25 gene
Chr 9
Friedrich’s ataxia Sx
Similar to SCD of cord:
Lateral corticospinal, dorsal column, spinocerebellar lesions:
B/l spastic paresis, proprioception, vibration sensation loss, ataxia, LMN sx, cerebellar ataxia, optic atrophy
HOCM
DM
High arched palate
Drugs exacerbating Myasthenia gravis
MP Questions LGBT
Macrolide
Procainamide, Penicillamine, Phenytoin
Quinolone, Quinidine
Lithium
Gentamicin
Beta blockers
Tetracyclines
How long does an AV fistula take to form
6-8 wks
Amiodarone induced thyrotoxicosis types
Type 1: excess iodine-induced synthesis. Goitre present. Treat with carbimazole or potassium perchlorate
Type 2: Destructive thyroiditis. Goitre absent. Treat with steroids
Myotonic dystrophy genetics
Aut Dom
Type 1 (DM1): CTG rpt at end of DMPK gene on Chr 19
Type 2 (DM2): rpt expansion of ZNF9 gene on Chr 3
Blood film on hyposplenism
Target cells
Howell-Jolly bodies
Pappenheimer bodies
Siderotic granules
Acanthocytes
IDA blood film
Target cells
Pencil pokilocytes
Myelofibrosis blood film
Tear drop poikilocytes
What is responsible for the plateau phase of a cardiac AP?
Slow Ca influx through L-type Ca channels
What is responsible for the rapid depolaration phase of a cardiac AP?
Rapid Na influx
What is responsible for repolarisation in a cardiac AP?
K efflux
What is responsible for restoration of ionic concentrations in a cardiac AP?
K influx with slow Na efflux, via the Na/K ATP-ase
Where are the majority of tumours in Zollinger-Ellison found?
1st part of the duodenum
2nd commonest - pancreas
Trastuzumab
Herceptin - HER2/neu receptor mAb
for metastatic breast Ca
Trastuzumab SE:
flu-like sx, diarrhoea
Cardiotoxicity, esp with anthracyclines - needs Echo before treatment
Which immunoglobulin type is raised in Alcoholic liver disease?
IgA
Which immunoglobulin type is raised in autoimmune hepatitis?
IgG
HLA association for autoimmune hepatitis
HLA B8
HLA DR3
Type I autoimmune hepatitis antibodies
ANA
anti-SMA
Type II autoimmune hepatitis antibodies
Anti-LKM1
Type III autoimmune hepatitis antibodies
Anti soluble liver kidney antigen ab
Complications of plasma exchange
HypoCa (due to citrate used as anticoagulant for extracorporeal system)
Metabolic alkalosis
Removal of systemic meds
Coagulation factor depletion
Immunoglobulin depletion
Indications for plasma exchange
GBS
Myasthenia
Goodpasture’s
ANCA-related vasculitis (if progressive renal failure or pulmonary haemorrhage)
TTP/HUS
cryoglobulinaemia
Hyperviscosity syndrome
Extra-articular features in IBD related to disease activity
Pauciarticular, asymmetric arthritis
Erythema nodosum
Episcleritis (more in Crohn’s)
Osteoporosis
Extra-articular features in IBD un-related to disease activity
Polyarticular symmetric arthritis
Uveitis (more in UC)
Pyoderma gangrenosum
Clubbing
PSC (more in UC)
Familial Mediterranean Fever inheritance
Aut rec
Familial Mediterranean Fever features
Recurrent Pyrexia + Polyserositis (pleuritis, peritonitis, pericarditis, arthritis), erysipeloid rash on lower limbs
Familial Mediterranean Fever Rx
Colchicine
Hungry bone syndrome
Uncommon complication post thyroidectomy if hyperPTH has been long-standing.
Results in hypoCa
High pre-op levels of PTH provide constant stimulus for high osteoclast activity. Once parathyroidectomy done, bones rapidly begin re-mineralisation to counter the chronic changes that osteoclasts have done
Coarctation of Aorta assx
Turner’s
Bicuspid aortic valve
Berry aneurysms
NF
Lithium toxicity precipitants
Diuretics (thiazides esp_)
ACE inhibitors/ARBs
NSAIDs
Metronidazole
Level at which lithium toxicity occurs and therapeutic level
> 1.5 - toxicity
0.4-1 - therapeutic range
Lithium toxicity features
CHAPS Coma
Coarse tremor
Hyperreflexia
Acute confusion
Polyuria
Seizure
Coma
Tunnel vision causes:
CHO RPG into the tunnel
Choroidoretinitis
Hysteria
Optic atrophy 2ndary to Tabes dorsalis
Retinitis pigmentosa
Papilloedema
Glaucoma
Otitis externa Rx
topical steroids + aminoglycoside
Anthrax Rx
ciprofloxacin
CYP450 inducers
CRAP GPS
carbamazepime
rifampicin
Alcohol (chronic)
Phenytoin
Griseofulvin
Phenobarbiton
Sulphonylureas/smoking/St John’s Wort
CYP450 inhibitors
SICKFACES.COM
Sodium valproate
Isoniazid
Cimetidine
Ketoconazole/fluconazole
Fluoxetine/sertraline
Alcohol (acute)/allopurinol/amiodarone
Ciprofloxacin/chloramphenicol
Erythromycin/clarithromycin
Sulphonamides
Cardiac/Liver failure
Omeprazole
Metronidazole
Which is more likely to develop T2DM - IFG or IGT
IGT
(IFG due to hepatic insulin resistance while IGT due to muscle insulin resistance)
Impaired fasting glucose diagnosis
Fasting glucose 6.1-7.0
Impaired glucose tolerance diagnosis
Oral glucose tolerance test (post-2hrs): 7.8-11.1
Sulfonylurea SE:
Hypo
Weight gain
SIADH
Cholesterol liver dysfunction
Peripheral neuropathy
Teratogenic
Meglitinides - when to give
basically work like sulfonylureas
For erratic lifestyles
Sulfonylurea MOA
Binds to ATP-sensitive K channels on beta cells, closing them
Increases glucose-INDEPENDENT insulin release
Thiazolidinediones SE
weight gain
fluid retention (worsened when given with insulin)
liver dysfunction
fractures
Bladder Ca
Gliptins SE
pancreatitis
GLP-1 mimetics SE
nausea, vomiting
Pancreatitis
Renal impairment
SGLT-2 inhibitors SE
urinary/genital infections
Fournier’s gangrene
Euglycaemic ketoacidosis
Lower-limb amputations
Weight loss
Pendred’s syndrome genetics
Aut Rec
SLC26A4 mutation in PDS gene
Chr 7
Pendred’s syndrome features
Defect in iodine organification
Progressive bilateral sensorineural deafness
Delay in academic progression
Exacerbated by head trauma
Mild hypothyroid/euthryoid with goitre
Pendred’s syndrome dx
perchlorate discharge test
Genetic testing
Audiometry
MRI (one and a half turns in cochlea instead of two and a half turns)
Pendred’s syndrome Rx
thyroid hormones
Cochlear implants
Pelvic inflammatory disease Rx
Oral ofloxacin + oral metronidazole
or
IM ceftriaxone + oral doxycycline + oral metronidazole
Chance of transmission after needlestick for HBV
20-30%
Chance of transmission after needlestick for HCV
0.5-2%
Chance of transmission after needlestick for HIV
0.3%
What stain should you use to diagnose Pneumocystis cariniii pneumonia?
Silver stain
Which foramen does the maxillary nerve go through?
Foramen rotundum
Which foramen does the mandibular nerve go through?
Foramen ovale
Which nerves go through through the jugular foramen?
CNs 9, 10, 11
Central causes of Horner’s
S’s - lesions directly in hypothalamus, brainstem, spinal cord, demyelination, neoplasms, syrinx
Stroke
Syringomyelia
multiple Sclerosis
Tumour
Encephalitis
How to distinguish between different causes of Horner’s
Central lesions have anhidrosis of face + arms + trunks
Pre-ganglionic have just anhidrosis of face
Post-ganglionic have no anhidrosis
Hydroxyamphetamine testing can also be done: pupils dilate in central/pre-ganglionic but not in post-ganglionic
Pre-ganglionic Horner’s causes
T’s
pancoasT’s
Tumour
Thyroidectomy
Trauma
Cervical Rib
Post-ganglionic Horner’s causes
C’s
Carotid artery dissection
Carotid aneurysm
Cavernous sinus thrombosis, Cluster headache
Pilocarpine action
muscarinic agonist
Timolol eye drops MOA
beta blocker –>
reduces aqueous production
Apraclonidine eye drops MOA
alpha 2 agonist
Reduces aqueous production + increases outflow
Latanoprost eye drop MOA
prostaglandin analogue
Increases uveoscleral outflow
Which cells produce pulmonary surfactant
Type 2 pneumocytes
What is the main functioning component of pulmonary surfactant?
Dipalmitoyl phosphatidylcholine (DPPC)
Severe AS features
narrow pp
slow rising pulse
soft/absent S2
S4
thrill
delayed ESM
longer ESM
LVH/failure (displaced apex beat)
Causes of Peripheral neuropathy with predominantly sensory loss
VALUE Diabetes
Vit B12 def
Amyloidosis
Leprosy
Uraemia
ETOH
Diabetes
Causes of Peripheral neuropathy with predominantly motor loss
GP’s CCD
GBS
Porphyria and lead poisoning (things down the haem biosynthesis pathway)
Charcot-Marie-Tooth
CIPD (chronic GBS)
Diphtheria
What is hazard ratio typically used for
analysing survival over time
Rheumatoid arthritis XR changes
Loss of joint space
Juxta-articular osteoporosis/osteopaenia
Soft-tissue swelling
Periarticular erosions
Subluxation
Vaughan Williams class 1a examples
quinidine
procainamide
disopyramide
Vaughan Williams class 1a MOA
blocks Na channels
Increases AP duration
Vaughan Williams class 1b examples
Lidocaine
Mexiletine
Tocainide
Vaughan Williams class 1b MOA
blocks Na channels
Reduces AP duration
Vaughan Williams class 1c examples
Flecainide
Encainide
Propafenodone
Vaughan Williams class 1c MOA
blocks Na channels
No effect on AP
Drug induced lupus causes
Most common: - PH
Procainamide
Hydralazine
Less common: - PIM
Isoniaizid
Minocycline
Phenytoin
Ataxic telangiectasia genetics
Aut Rec
DNA repair enzyme defect
Wiskott-Aldrich syndrome genetics
X recessive
WASP gene defect
Red flag features when assessing for IBS
Rectal bleed
weight loss (unexplained)
FHx of bowel/ovarian Ca
Onset>60yrs of age
Homocystinuria genetics and defect
Aut Rec
Cystathionine beta synthase def
Homocystinuria features
Hair: Fine, fair hair
Body/Bones: Marfanoid, Osteoporotic, Kyphotic
Neuropsych: LD, Seizures
Eyes: Downwards (inferonasal) lens dislocation, Severe myopia
CVS: Arterial + venous thromboembolisms
Skin: Malar flush, Livedo reticularis
Homocystinuria Ix
plasma, urine homocysteine conc high
Cyanide-nitroprusside test +ve
Homocystinuria Rx
vit B6 (pyridoxine) supplements
Phenylketonuria Genetics + Defect
Aut Rec
Chr 12
Phenylalanine hydroxylase def
Phenylketonuria features
General: Fair hair, Blue eyes
Urin: Musky
Neuropsych: LD, Seizures
Skin: Eczema
Phenylketonuria Ix
Guthrie’s test
Hyperphenylalaninaemia
Urinary phenylpyruvic acid
Alkaptonuria genetics + defect
Aut Rec
HGD def
Alkaptonuria Sx
Eyes: pigmented sclera, corneal deposits
Urine: dark urinary homogentisic acid (dark urine on standing), Renal stones
Bones: intervertebral disc calcification
Alkaptonuria Rx
Vit C
restrict phenylalanine and tyrosine
Beckwith-Wiedemann syndrome features
Assx: Wilm’s
Organomegaly
Abdo wall defects
Neonatal hypoglycaemia
Von Gierke’s disease defect
Glucose-6-phosphatase defect –> hepatic glycogen accumulation
Von Gierke’s features
Hypoglycaemia
Lactic acidosis
Hepatomegaly. (Von Gierke’s got a big liver - due to hepatic glycogen accumulation)
Pompe’s disease defect
Lysosomal alpha 1,4 glucosidase def
Pompe’s disease features
Cardiomegaly (Pompey’s got a big heart)
Cardiac, hepatic, muscle glycogen accumulation
Cori disease defect
Alpha 1,6, glucosidase defect
Cori disease features
Muscle dystonia
Hepatic, cardiac glycogen acccumulation
