Week 16 extras and Derm Flashcards
(37 cards)
Epilepsy causes
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.
Epilepsy features
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 After an acute brain insult, AEDs to treat provoked seizures should be withdrawn, unless unprovoked seizures occur, likely with neurodeficit or structural abnormality.
Types of seizures
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
Epilepsy treatment summary
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
Clotting screen results
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
Von Willebrand disease
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.
Thrombotic thrombocytopenic purpura (what, signs, management)
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.
Immune thrombocytopenia (what, signs, management)
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.
Haemolytic vs sideroblastic anaemia diseases
Haemolytic- G6PD, thalassemia, sickle, spherocytosis, autoimmune conditions
Sideroblastic- Pearson, wolfram, erythropoietic protoporphyria, myelodysplastic syndrome, lead, zinc, alcohol, progesterone, hypothermia. Vitamin b6/pyridoxine = helpful.
Acute and long term stroke management
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.
Initial and long term heart failure management
initial- eg HF with pulmonary oedema- O2, furosemide, morphine, dopamine.
Later- ACE, betas, loops, spironolactone, digoxin if AF.
Arrhythmia drugs
VT- amiodarone with lidocaine, WPW- propanolol, Afib- metoprolol, amiodarone, digoxin. VF- amiodarone, Aflut- verapamil hydrochloride, torsades- magnesium
Primary and secondary HTN management
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.
Early management for unstable angina or acute NSTEMI
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.
STEMI early management
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.
Secondary prevention of STEMI
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.
Effects of alcohol damage
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.
Wernicke-Korsakoff syndrome
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.
Signs of Wernicke-Korsakoff syndrome
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.
Signs of wet beriberi
Inc HR, vasodilation, inc JVP, PN Dyspnoea, oedema, dilated cardiomyopathy
Causes of infertility
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.
What is measured in ovulation tests?
LH surge before ovulation. Ovulation is considered 28-36 hours after the beginning of LH raise or 8-20 hours after it’s peak.
Reasons for anovulation
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.
PCOS diagnosis
2/3 of oligomenorrhoea, hyperandrogenism, polycystic ovarian morphology = antral follicles >11 per ovary, and/or ovarian volume >9ml per ovary.
