Week 16 extras and Derm

Question 1

Epilepsy causes

Answer 1

To diagnose epilepsy- 2+ seizures more than 24hours apart.

Causes- idiopathic ( more likely if focal), cerebral infarct, haemorrhage, head injury (more likely if lost consciousness + was over 30 mins), meningitis, encephalitis, Alzheimer’s, autoimmune disease, brain tumour, metabolic imbalance, drugs and alcohol, benzos, tricyclics, isoniazid, phenothiazines.

Question 2

Epilepsy features

Answer 2

Sudden death = more likely when asleep, young adult, tonic-clonic seizures, neurological comorbidity and AED polytherapy.

Features if genetic- childhood onset, triggered by sleep loss or alcohol, early morning onset, short absence seizures on EEG, aura, focal motor symptoms.

Skin associations- cafe-au-lait = NF, Port-wine stain = Sturge-weber, adenoma sebaceum= tuberous sclerosis.

Provoked seizures= within 7 days of an acute condition eg encephalitis, drugs and alcohol. After an acute brain insult, AEDs to treat provoked seizures should be withdrawn, unless unprovoked seizures occur, likely with neurodeficit or structural abnormality.

Question 3

Types of seizures

Answer 3

Tonic-clonic seizure- whole body stiffens, loses consciousness, then convulsions.

Absence- loss of consciousness/awareness temporarily

Myoclonic seizure- sudden contraction of the muscles, which causes a jerk

Tonic- brief loss of consciousness + stiff and fall to ground

Atonic- limp + collapse with just very brief loss of consciousness

Simple focal seizures- activity starts and stays in one part of the brain with consistent symptoms in the episode

Complex focal seizure- affects a region or moves, eg temporal lobe epilepsy. This type can affect your levels of consciousness + shows more complex behaviour.

Focal -> generalised = secondary generalised seizure

Question 4

Epilepsy treatment summary

Answer 4

Tonic-clonic seizure- sodium valproate, lamotrigine

Absence- ethosuximide or sodium valproate

Myoclonic- Sodium valproate, topiramate, levetiracetam

Atonic- Sodium valproate

Focal seizures- gabapentin and pregabalin

Sodium valproate- teratogenic

Question 5

Clotting screen results

Answer 5

Vit K or warfarin- inc PT and APTT
Haemophillia- inc APTT
vWBR- inc APTT and TT
DiC- Inc PT, APTT, TT, dec platelets
IT/TTP/HUS- inc TT, dec platelets

Question 6

Von Willebrand disease

Answer 6

Clotting disorder that affects females more but is equally sex-inherited. Types 1,2,3.

T2 shows the characteristic monocutaneous bleeding.

T1 is usually not diagnosed until adulthood. Nosebleeds, bleeding gums, easy bruising, pregnancy complications can occur. T1 is milder and 70-80% of all cases. Factor 8 is also reduced.

T3 is recessive, unlike 1 and 2. Shows monocutaneous bleeding, compartment and joint bleeding, joint damage, haematomas.

If mild, treat with desmopressin acetate, like haemophillia A bc it increases factor 8. If more severe, require factor replacement therapy of vwf and 8.

Question 7

Thrombotic thrombocytopenic purpura (what, signs, management)

Answer 7

Clotting disorder that gives microangiopathic haemolytic thrombocytopenia, neurological/renal issues and a fever. Due to a deficiency in ADAMTS1 that cleaves von willebrand factor. Occurs more commonly in females.

Signs- epistaxis/bruising/petechiae/gingival bleeding/haematuria/menorrhagia/GI bleeding/retinal haemorrhage/haemoptysis, headache, dysarthria, encephalopathy, dysphasia, fever, jaundice/haemolytic anaemia, proteinuria, inc creatinine and urea, arrhythmia, hypotension, splenomegaly, purpuric rash, schistocytes.

Management- iv plasma exchange/plasmapheresis to remove antibodies and supply von willebrand factor within 4-8 hours, with fresh frozen plasma if delayed. Can also use prednisone and/or rituximab- if refractory, relapsing immune ttp or cardiac/neuro signs.

Question 8

Immune thrombocytopenia (what, signs, management)

Answer 8

Immune thrombocytopenia = idiopathic thrombocytopenic purpura. Autoimmune disorder with reduced numbers of circulating platelets, can be caused by other autoimmune conditions eg antiphospholipid syndrome, SLE, viral infections, h.pylori. Has , 100 x 10-9/L thrombocytes. Recovers spontaneously.

Can be asymptomatic, petechiae, bruising, nosebleeds, haematuria, GI bleeds, menorrhagia and occasionally intracranial bleeds.

First line management - if platelet count is too low- prednisone, ivig, iv antiD, rituximab, high dose dexamethasone.

Question 9

Haemolytic vs sideroblastic anaemia diseases

Answer 9

Haemolytic- G6PD, thalassemia, sickle, spherocytosis, autoimmune conditions

Sideroblastic- Pearson, wolfram, erythropoietic protoporphyria, myelodysplastic syndrome, lead, zinc, alcohol, progesterone, hypothermia. Vitamin b6/pyridoxine = helpful.

Question 10

Acute and long term stroke management

Answer 10

Alteplase within 4.5 hours or mechanical thrombectomy for ACA within 6hrs and 12hrs for PCA. Follow with aspirin.

HALTSS- sort with antihypertensives after two weeks, antiplatelets- clopidogrel then warfarin after 2 weeks. Lipids- atorvastatin. TSS= lifestyle factors.

Question 11

Initial and long term heart failure management

Answer 11

initial- eg HF with pulmonary oedema- O2, furosemide, morphine, dopamine.

Later- ACE, betas, loops, spironolactone, digoxin if AF.

Question 12

Arrhythmia drugs

Answer 12

VT- amiodarone with lidocaine, WPW- propanolol, Afib- metoprolol, amiodarone, digoxin. VF- amiodarone, Aflut- verapamil hydrochloride, torsades- magnesium

Question 13

Primary and secondary HTN management

Answer 13

primary- ACE/ARB if t2 diabetes and less than 55 and not african. then add CCB or thiazide, then add the other. Then add spironolactone if potassium ,4.5mmol/L

If over 55, stage 2 or african- CBB or thiazide, then with ACE/ARB or thiazide, then combine CCB, thiazide ,ACE, then if potassium ,4.5mmol/L consider adding an alpha or beta blocker.

If a case of secondary HTN- ACE< beta, CCB, thiazide , or loop furosemide, doxazocin, eplerenone, spironolactone.

HTN = 140/90, 160/100, 180/120. masked is less than 140/90 in clinic. Whitecoat is 20/10 difference.

Question 14

Early management for unstable angina or acute NSTEMI

Answer 14

After 300mg aspirin, antithrombin therapy: fondaparinux if not a high bleeding risk. If significant renal impairment creatinine over 215 then use unfractionated heparin instead. If high bleeding risk, use another antithrombotic.

Question 15

STEMI early management

Answer 15

Assess suitability for percutaneous coronary intervention or fibrinolysis. Primary PCI is not recommended when symptom onset is more than 12 hours and the patient is asymptomatic.

Initial drug therapy is 300mg aspirin.

Consider coronary angiography for those who presented over 12 hours ago with still ongoing ischemia or cardiogenic shock.

If someone has PCI- give dual antiplatelet therapy of prasugrel with aspirin or clopidogrel with aspirin if already taking one of the two latter anticoagulants.

Unfractionated heparin is given with a PCI.
When giving fibrinolysis if a PCI can’t be given, give antithrombin at the same time.

If can’t give either therapy- give ticagrelor with aspirin, unless high risk for bleeding then give clopidogrel and aspirin.

Question 16

Secondary prevention of STEMI

Answer 16

ACE, dual antiplatelet eg aspirin and clopidogrel, betablocker, statin. x routinely offer ccb to reduce cardiovascular risk after MI. If acute MI and HF give aldosterone whilst monitoring renal function and serum potassium.

Question 17

Effects of alcohol damage

Answer 17

Vascular dilation, cholesterol balance, HTN, inflammation, stroke, ADH suppression and fluid loss, inhibitory arousal, impotence, testicular atrophy, shrinking of prostate and seminal vesicles, stomach inflammation, diarrhoea/decreased absorption, fatty liver, alcoholic hepatitis, cirrhosis, holiday heart syndrome, triglyceride build up, acetaldehyde accumulation, scarring.

Question 18

Wernicke-Korsakoff syndrome

Answer 18

Forms of dry beriberi thiamine deficiency and alcohol misuse. Triad = mental confusion, ataxia, ophthalmoplegia. Korsakoff’s syndrome = a late progression from wernicke’s encephalopathy. This syndrome is signs of both.

Areas of alcohol related neuronal loss matches with WKS= thalamus, hypothalamus and mammillary bodies. Other causes are bowel obstruction laparotomy, bariatric surgery, Chronic subdural haematoma, chemo, hyperemesis gravidarum, mercury poisoning, AIDs, malnutrition.

Question 19

Signs of Wernicke-Korsakoff syndrome

Answer 19

Double vision, eye movement (congugate gaze palsy, nystagmus, bilateral lateral rectus palsy, eye droop, generally uncoordinated, hallucinations, polyneuropathy, reflex change, (wernicke’s encephalopathy) and loss of memory, can’t create new memories, confabulation/false memories and strange answers (korsakoff’s syndrome).

Sort with oral, IM or IV thiamine.

Question 20

Signs of wet beriberi

Answer 20

Inc HR, vasodilation, inc JVP, PN Dyspnoea, oedema, dilated cardiomyopathy

Question 21

Causes of infertility

Answer 21

Early follicular phase: raised FSH = ovarian failure, raised LH = PCOS, low FSH+LH= h-P failure.

Can also measure fertility by mid-cycle ultrasound with follicle tracking, antral follicle count, endometrial thickness.

Question 22

What is measured in ovulation tests?

Answer 22

LH surge before ovulation. Ovulation is considered 28-36 hours after the beginning of LH raise or 8-20 hours after it’s peak.

Question 23

Reasons for anovulation

Answer 23

Hypothalamic/pituitary failure- hypogonadotropic hypogonadism, weight loss, kallman’s syndrome, hyperprolactinaemia, thyroid dysfunction, hypopituitism.

These show Dec FSH Dec LH Dec E2/oestradiol. If underweight, FSH could be normal.

H-P dysfunction- the most commons cause- PCOS- shows n/Dec FSH, n/Inc LH, nE2, Dec SHBG, Inc testosterone, Inc androgen index (T/SHBG)

Ovarian failure- premature ovarian insufficiency, chemo. Really Inc FSH, Inc LH, dec E2.

Beware of mid cycle surge = inc fsh, really inc LH and inc E2.

Question 24

PCOS diagnosis

Answer 24

2/3 of oligomenorrhoea, hyperandrogenism, polycystic ovarian morphology = antral follicles >11 per ovary, and/or ovarian volume >9ml per ovary.

Question 25

Treatment for anovulation

Answer 25

Correct BMI,
PCOS = clomifene citrate/ letrozole oestrogen antagonists, metformin, ovarian drilling, gonadotrophin/FSH injections.
Hyperprolactinemia = bromocriptine, cabergoline
Ovarian dysfunction = ovum donation
Hypogonadotrophic hypogonadism = treat underlying illness and then give pulsatile GNRH/LH+FSH.

Question 26

Reasons for sperm dysfunction

Answer 26

Lifestyle
Klinefelter's, XO
Varicocele
STIs
CABVD
Ecoli/ strep faecalis/ appendicitis

Question 27

Normal semen analysis results and name related tests

Answer 27

Volume > 1.5ml concentration > 15x10-6/ml motility over 40% normal morphology 4% or more with over 20mil normal motile sperm.

Chlamydia antibodies, HSG, Hy-co-sy, laparoscopy and dye test.

Question 28

Endometriosis

Answer 28

Ectopic endometrial glands and stroma causes ovarian dysfunction, raised prostaglandins, prostacyclins, tissue factor and adhesions. Give clomiphene/letrozole to induce ovulation.

Question 29

Stages of IVF and risks

Answer 29

Down regulate LH, induce ovulation with exogenous FSH, BhCG to trigger ovulation, oocyte recovery +/- intracytoplasmic sperm injection, embryo culture and transfer, luteal phase support with added progesterone.

~Some of these steps can be omitted.

Risks are multiple pregnancy, ovarian hyperstimulation syndrome, haemorrhage and infection.

Question 30

Psychologically mimicking illnesses for depression (3), mania (1), anxiety(3), psychosis(2)?

Answer 30

Depression: Addison’s( Addisonian crisis = dec HTN dec Na and glucose inc K), hypothyroidism/myxedema madness, haemochromatosis (+ferritin +transferrin, recessive).

Mania: Cushing’s

Anxiety: pheochromocytoma, hyperthyroidism, thyroid nodules (-TSH +T4, give carbimazole/propylthiouracil)

Psychosis: Wilson’s disease (- caeruloplasmin), Acute intermittent porphyria( diagnose with ALA and PBG).

Question 31

Cellulitis and Erysipelas

Answer 31

Cellulitis is an acute spreading infection of the skin with visually indistinct borders that principally involves the dermis and subcutaneous tissue. It is characterised by redness, swelling, heat, and tenderness, and commonly occurs in an extremity.

Erysipelas is a distinct form of superficial cellulitis with notable lymphatic involvement. It is itchy, raised and sharply demarcated from uninvolved skin.

Check for sepsis first. Erysipelas should be treated in the same way as cellulitis. Flucloxacillin 500 mg four times daily (in adults) is usually given as first-line in uncomplicated infection. Erythromycin 500 mg four times daily, clarithromycin (500 mg twice daily) or doxycycline 200 mg on the first day and then 100 mg daily for 5-7 days can be used if the patient is penicillin-allergic.

Alternative first-line antibiotic if the infection is near the eyes or nose is co-amoxiclav 500/125 mg three times a day orally for 7 days. If the person is allergic to penicillin they can have clarithromycin 500 mg twice a day for 7 days with metronidazole 400 mg three times a day for 7 days.

Question 32

Signs of cranial abscess

Answer 32

Common presenting symptoms include 
changes in mental state (drowsiness, confusion), 
grand mal seizures, 
nausea and vomiting, 
neck stiffness.
Fever,
Focal motor or sensory deficits,
Raised blood pressure and bradycardia associated with raised intracranial pressure.
Papilloedema,
Ataxia,
Bulging fontanelle in infants.

A suddenly worsening headache, followed by emerging signs of meningism, are often associated with rupture of the abscess.

Question 33

Signs of Lung abscess

Answer 33

Onset of symptoms is often insidious (more acute if following pneumonia).
Spiking temperature with rigors and night sweats.
Cough ± phlegm production (frequently foul-tasting and foul-smelling and often blood-stained).
Pleuritic chest pain.
Breathlessness.
Tachypnoea.
Tachycardia.
Finger clubbing in chronic cases.
Dehydration.
High temperature.
Localised dullness to percussion (if consolidation is also present or effusion).
Bronchial breathing and/or crepitations (if consolidation is present).
Also look for signs of severe periodontal disease and infective endocarditis.

Can be a secondary to another infection, eg hepatic abscess.

Question 34

Kallmann syndrome

Answer 34

Kallmann syndrome (KS) is a genetic disorder that prevents a person from starting or fully completing puberty. To distinguish it from other forms of hypogonadotropic hypogonadism, Kallmann syndrome has the additional symptom of a total lack of sense of smell (anosmia) or a reduced sense of smell.

Other signs- micropenis, cryptorchidism, cleft palate/lip, singular kidney, skeletal defects, neural hearing impairment, ataxia, coloboma or ptosis, colour blindness.

Question 35

Hypogonadotrophic hypogonadism causes

Answer 35

HPA issue bc dec GNRH. Congenital or acquired: x-linked recessive kallman’s, sarcoiodosis, pituitary adenomas, craniopharyngiomas, hyperprolactinemia most commonly. Use HCG and FSH.

Question 36

Hyperprolactinemia causes

Answer 36

Inc prolactin in blood. Caused by stress, pregnancy/breastfeeding, tumours, rathke’s cyst, prolactinoma, acromegaly, loran syndrome, CKD, hypothyroidism, cirrhosis, epilepsy, dopamine receptor blockers, ranitidine, cimetidine, TCAs, SSRIs, verapamil.

Question 37

Hypopituitism causes

Answer 37

Sheehan’s syndrome, haemochromatosis, sarcoidosis, infection, radiation and tumours.