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Core Medicine (Neuro (GI (Emergency)), Resp (Rheum (Cardio (GU))), Get…

- - - - GU
- - - - Oncology
        
        CBD A&E
- - - - Bacterial- cloudy/turbid appearance , high neutrophils, high protein, low glucose
        Viral- clear appearance, high lymphocytes, normal/high protein, normal glucose
- - - - Focal
        
        Types
        
        Simple
        
        Arise from frontal lobe (motor cortex), assoc.w/jerky movements
        
        Jacksonian March= progression of location of simple focal seizure in brain which presents as 'march' of motor presentation from distal part of limb towards ipsilateral face
        
        Complex
        
        Arise from temporal lobe, assoc.w/ unpleasant sensations
        
        PPh: only one hemisphere involved
        Mx: Carbamazepine- inhibits pre-synaptic Na+ channels so prevents axonal firing
      - Generalised
        
        Types
        
        Myoclonic
        
        Isolated muscle jerking
        
        *Tonic-clonic
        
        Sudden onset rigidity (tonic phase) followed by convulsions (clonic phase)
        episodes last up to 120 seconds, assoc.w/ tongue biting and incontinence
        
        Absence
        
        Present in childhood, cease activity, blank stare
        
        PPh: both hemispheres involved, always involves disturbance to/LOC
        Mx: sodium valproate !SE teratrogenic
- - - - Chronic AI condition, inflammatory demyelinating disease.
        F>M, 20-40yo, assoc w/EBV infection, genetic
        T cell activation --> B cell + macrophage activation --> inflammation, demyelination, axonal destruction
      - Relapsing-remitting: random attacks over a number of years, no disease progression between attacks
        Chronic progressive: slow decline in neurological functions from onset
  - - - UMN
        
        S&S: increased muscle tone, hyper-reflexia, positive babinski, muscle weakness
        
        PPh: UMN= neurone located entirely in CNS, cell body located in primary motor cortex.
        Causes UMN pathology: neurodegenerative (MND), vascular (CVA), inflammatory (MS), spinal compression (tumour)
      - LMN
        
        PPh: LMN= neurone that carries signals to effector, cell body located in brain stem/spinal cord
        Causes LMN pathology: brainstem/spinal cord (MND, spinal cord compression, vascular), spianl roots (disc prolapse, tumour), peripheral nerve (demyelination), NMJ (MG)
        
        S&S: reduced muscle tone, hypo-reflexia, muscle wasting, fasciculations
    - - Amyotrophic lateral sclerosis 50% (combined LMN and UMN)
        Progressive muscular atrohpy 25% (anterior horn cell lesions- distal muscles >proximal)
        Bulbar palsy 25% (palsy of tongue / muscles of chewing+swallowing)
    - - Riluzole- inhibits glutamate release and slows progression, ventilatory suport, PEG feed
- - - - 15 mins-3 hours
        Unilateral, pain around eye, severe/very severe pain,
    - - 4-72 hrs. Triggers CH-cheese, O-OCP, C-caffeine, OL-alcohol, A-anxiety, T-travel, E-exercise
        Unilateral, throbbing, mod/severe pain, aggravated by physical activity ?photophobia +/- phonophobia, nausea (NOT vomiting)
        20% are with aura = visual (flashing lights), sensory (tingling hands/feet), language or motor aura
        Mx: avoid triggers, NSAIDs, triptans, anti-emetics, propanolol (preventative)
    - - 30 mins-7 days
        Bilateral, pressing/tight, mild/mod pain, NOT aggravated by physical activity
  - - - S&S: Thunderclap, maximum severity in seconds
        Ix: CT head, cerebral angiography
        Mx: resuscitation, nimodipine (CCB),
    - - Criteria: headache >15 days/month, regular use >3mo >1symptomatic tx drug, headache worse during drug use
    - - S&S: pyrexia, neck stiffness, photophobia, non-blanching purpuric rash
        Ix: FBC, blood cultures, throat swabs, LP, CT head
    - - Giant cell arteritis
- - - - Lower limb: weakness, loss of sensation, gait apraxia (unable to initiate)
        Other: incontinence, drowsiness, decreased spontaneous speech
    - - Upper limb: weakness, loss of sensation
        Speech: aphasia, dysphasia
        Other: haemianopia, facial droop
    - - Vision: field defect, cortical blindness,
        Recognition: agnosia (unable to identify objects), prosopagnosia (unable to recognise faces)
        Other: dyslexia, headache
- - - - ?tranexamic acid / O- blood if you you think they are bleeding (C)
        FAST scan (good for B/ C)
        Catheterise the patient (part of E)
        Log roll patient (part of E)
        Carry out a second survey
    - - Obtain WBCT
        Arterial line
        Rapid sequence induction
- - - - Staging (blood loss): Class 1 (10-15%), Class 2: (15-30%), Class 3: (30-40%), Class 4 (40%)
      - Compensated shock: baroreceptor reflexes increase heart contractility, tachycardia and vasoconstriction which maintains CO and BP, they also lead to release of vasopressin, aldosterone and renin
        Progressive/uncompensated shock: myocardial depression, failure of vasomotor reflexs, failure of microcirculation. Increased capillary permeability, sludging and thrombosis. Cellular dysfunction and lactic acidosis.
        Irreversible shock: failure of vital organs with inability to recover
    - - O2, secure venous access early (before circulatory collapse)
        Reuscitation with crystalloid e.g normal saline or hartman's
        If haemorrhage give blood ASAP
        Serious blood loss- consider REBOA (resuscitative endovascular balloon occulsion of aorta)- balloon introduced via femoral into aorta which is inflated to cut of blood supply above haemorrhaging point
    - - Percussion
        Tension= hyperresonant
        Haemothorax= dull
      - Thoracocentesis= 2nd intercostal space mid-clavicular line
        Thoracotomy- pre-hospital, put a hole in your chest (open pneumothorax better than tension)
        Chest drain- 5th intercostal space mid-axillary line 'triangle of safety'
- - - - Cardiogenic
        
        Massive MI or other causes of primary cardiac failure
      - Obstructive
        
        Massive PE, tamponade, tension pneumothorax
      - Distributive
        (vasodilation +/- leakage
        from endothelium)
        
        Septic
        
        Anaphylactic
        
        Neurogenic
- - - - 1 (benign paediatric)
      - 2 (pre-malignant) - young adults, present with seizure
      - 3 (anaplastic astrocytoma)
      - 4 (glioblastoma multiforme)
        
        Mx: resective surgery, adjuvant chemo (temozolomide), palliative care
        
        Prognsosis
        
        Good
        
        Age <45, secondary GBM, MGMT 'mutant' (responds well to chemo)
        aggressive surgery, good neuro function post-surgery
        
        Poor
        
        Age >50, primary GBM, MGMT 'wild type' (no response to chemo)
        non-radical surgery, poor neurol function post-surgery
        
        PPh: initial genetic error of glycolysis --> IDH 1 mutation --> excessive build up of 2 hydroxyglutarate --> genetic instability in glial cells triggered
- - - - Acute- vascular / inflammatory / toxic
      - Subacute- inflammatory / toxic / nutritional / systemic illness
      - Chronic- hereditary/ metabolic
    - - ?systemic disease = bloods (FBC, ESR, U&E, LFT)-
      - ?specific cause- BM, B12, TFT, electrophoresis (paraprotein), autoantibodies (ANCA, ANA)
      - ?neuropathy- nerve conduction studies (NCS) and Electromyography (EMG)
    - - NCS / EMG
        
        Demyelinating neuropathy - GBS- slow conduction / no denervation
        
        Axonal neuropathy- drugs e.g vincristine- normal conduction/ evidence of denervation
- - - - Fine, fast, postural tremor seen with anxiety
    - - Hyperthyroidism, high intake of alcohol/caffeine, SE of beta agonists
    - - Coarse / violent, assoc with lesion of red / subthalamic nucleus.
        Mostly caused by cerebrovascular disease or MS
        Essential tremor is most common cause of action tremor
    - - Parkinson's- slow, coarse tremor worst at rest, reduced by voluntary movement
        Usually in upper limbs, usually asymmetrical
- - - - Vasovagal
        
        Most common, precipitated by stimulation of PNS e.g emotional pset, unpleasant sights
        Pre-syncopal phase - light-headed, tinnitus, nausea, vision 'greying out'
        S&S- happens when standing, pale, slump to floor, rapid recovery
      - Cardiac
        
        Mechanical e.g left ventricular outflow obstruction (AS, hypertrophic cardiomyopathy)
        
        Dysrthythmia e.g complete heart block
      - Orthostatic
        
        Drugs- anti-HTN, diuretics, TCAs
        
        Low volume e.g dehydration, diarrhoea, haemorrhage
    - - Generalised
        
        Most common is tonic-clonic
        Always involve a disturbance / loss of consciousness
      - Focal
        
        Simple
        
        Arise from frontal (motor) cortex, assoc w/jerky movements
        
        Complex
        
        Arise from temporal lobe, assoc. w/unpleasant sensations
    - - Hypoxia, hypovolaemia, hypoglycaemia,
        Toxins e.g opioids, alcohol, CO, benzodiazepines, TCAs
        Metabolic- T2 respiratory failure, hepatic/renal failure,
        Hypothermia or hyperthermia
    - - Intracranial haemorrhage e.g SAH,
        Ischaemia e.g thrombosis/embolism,
        Trauma e.g conciussion, haemorrahge (extra/subdural or intracranial),
        Infections (meningitis, encephalitis, cerebral malaria),
        Primary or secondary tumours,
        Hypertensive encephalopathy
        Cerebral abscess
        Cerebral lymphoma
- - - - Bradycardic - ?syncope ?heart block
        Irregular- sudden-onset AF
        Tachycardic- ?supreventricular/ventricular tachycadia ?post-seizure tachycardia
    - - Hypotension- ?septicaemia ?acute MI
        Standing and lying BP ?postural hypotension (>20mmHg change in systolic BP)
    - - Raised- ?meningitis ?SAH
  - - - Structural heart disease ?valve disease ?VSD post-MI ?cardiac tamponade
    - - Bruits ?embolic cerebrovascular accident
- - - - Type I hypersensitivity reaction occuring when allergen reacts with IgE antibodies on mast cells / basophils causing rapid release of stored histamine and synthesis of newly formed mediators. Anaphylactoid reactions are not IgE-mediated but cause similar mast cell activation.
        Causes: drugs (penicillin / CT contract), latex, stings, eggs, peanuts, strawberries
    - - Cardio= tachycardia, hypotension
        Resp= cyanosis, wheeze
        Swelling= tongue, lips, lids, larynx
        Skin= urticharia, itching, sweating
        Other= N+V, diarrhoea
    - - Acute mx
        
        ABCDE
        Secure airway, give 100% O2
        Adrenaline 0.5mg 1:1000 IM every 5 mins
        Chlorphenamine 10mg IV + Hydrocortisone 200mg IV
        0.9% saline, 500ml / 15 mins up to 2L
        If wheeze- tx for asthma ?ventilator
        If still hypotensive - admit to ITU, IV adrenaline +/- aminophylline + salbutamol nebs
      - Further mx
        
        Admit to ward and monitor ECG
        MedicAlert bracelet
        Epipen (0.3mg adrenaline)
        Skin-prick test
- - - - Trauma- bruising, MI- ECG changes, Unstable angina- stress ECG,
    - - TB, pneumonia, effusion, PE, pneumothorax
  - - - Genetic abnormality increase clotting (factor V leiden / antibody protein C resistance)
        Acquired causes of pro-thrombotic state (anti-phospholipid syndrome/ antibody protein C resistance)
    - - Autosomal dominant gene mutation causing thrombophilia, increased tendency to clot
- - - - ?Tuberculosis / Lung CA
    - - ?Small pleural effusions
    - - ?Left lower lobe collapse- sail sign
- - - - Respiratory acidosis
        
        e.g COPD (retention Co2), sedative drugs/atelectasis (hypoventilation)
    - - Metabolic acidosis
        
        e.g DKA, severe diarrhoea, severe dehydration, prolonged lack of O2 from shock / HF
  - - - Respiratory alkalosis
        
        e.g panic attack / asthma (hyperventilation)
    - - Metabolic alkalosis
        
        e.g vomiting
- - - - Vit B1 (beri-beri)- 'dry'= neuropathy, 'wet'= cardiac failure
        Vit C (Scurvy)- corckscrew hairs, perifollicular haemorrhage, swollen/bleeding gums, tooth loosening
        Vit D- proximal myopathy, bone pain, malaise
        Vit K- bruising
- - - - Primary: GCA , talayasu's arteries
        Secondary: RA, ankylosing spondylitis, bechets syndrome, syphilis
    - - Primary: kawasaki, classic polyarteries nodosa
        Secondary: hepatitis B and C
    - - Primary: wegner's granulomatosis, churg-strauss syndrome, microscopic polyangitis (EXTRA)
        Secondary: RA, SLE, sjogren's, HIV drugs (sulphonamides, penicillins, thiazides)
    - - Primary: henoch-schonlein purpura, essential mixed cryoglobulinaemia
        Secondary: RA, SLE, sjogrens, CA, lymphoma, TB, group A strep, drugs (sulphonamides, penicillins, thiazides),
    - - These assoc. w/ ANCA antibodies, renal impairment and are responsive to immunosuppression with cyclophosphamide
  - - - RFs: women, child-bearing age, afro-caribbean / asian
        Trigger: EBV
      - Autoantibodies made against autoantigens (e.g ANA), results in polycolonal B-cell secretion of pathogenic autoantibodies and immune complex deposits in sites such as kidneys
    - - Renal: persistent proteinuria, cellular casts
        Serositis: pericarditis / pleuritis
        Haem: haemolytic anaemia, leukopenia, lymphopenia, thrombocytopenia
        CNS: seizures, psychosis
        Other antibodies: anti-smooth muscle, antiphospholipid
      - Non-specific: malaise, fatigue, myalgia, fever, lymphadenopathy, wt loss, alopecia
      - Diagnostic= DUAL RASH FACE
        Discoid rash, Ulcers (mouth), ANA+, Light sensitivity
        Renal disorder, Anti-dsDNA, Serositis, Haematological
        Flushed (malar rash), Arthritis, CNS disorder, ESR raised(normal CRP)
    - - Anti-dsDNA, complement C3/C4 depleted, ESR raised, CRP normal
    - - Severe flare: IV cycylophosphamide + high-dose prednisolone
        Skin sx: topical steroids, suncream
        Maintanence: NSAIDs, hydroxychloroquire
        Other: rituximab
- - - - Shockable rhythm
        (VF / pulseless VT)
        
        Given after 3rd shock
        1mg IV 1:10,000
        (1mg in 10ml solution, give whole 10ml flush)
        Repeat every 3-5 mins
      - Non-shockable rhythm
        (aystole / pulseless electrical activity)
        
        Given ASAP
        1mg IV 1:10,000
        (1mg in 10ml solution, give whole 10ml and flush)
        Repeat every 3-5 mins
    - - IM 0.5mg 1:1000
        Anterolateral thigh, mid way between knee and hip
- - - - SE peripheral oedema
    - - SE of electroly disturbance- hyponatraemia, hypokalaemia, hypomagnesaemia,
        and (less commonly) hypercalcaemia
    - - Given in PE, stops new thrombus being formed but existing thrombus need to be broken down by body's intrinsic fibrinolytic action, this can take several days
  - - - Murmurs- innocent flow murmur normal
        ECG- sinus rhythm with left axis deviation
        Resp/blood gases- higher RR--> increased minute volume ventilation--> lower PaCO2
    - - Position mother in left lateral position.
        Improves venous return to heart by ensuring feotus not pressing on IVC
        If spontaneous circulation not returned in 5 minutes, emergency Csection indicated
- - - - Cardiac failure (echo, ECG, echo)
        Renal failure (U+E)
        Iatrogenic fluid overload
    - - Serum
        albumin
        
        Low
        
        Proteinuria
        
        Nephrotic syndrome (U+E, albumin, urine dip)
        
        No proteinuria
        
        Hepatic failure (albumin, LFTs)
        Malnutrition (albumin)
        
        Normal
        
        Drugs e.g NSAIDs / CCBs
        Lymphatic / venous obstruction
        Reassess JVP
- - - - Time <8hr and above tx line= n-acetylcystine
      - Time >8hr and suspected large dose (7.5g)= start acetylcystine and stop if INR/ALT normal
      - Time >15hr / unknown / staggered = get advice, tx may help
      - N-acetylcystine
        
        This is a precursor to glutathione so increase stores and increase detox of paracetamol
        IVI 150mg/kg in 200ml 5% dextrose over 15 mins
        Then 50mg/kg in 500ml 5% dextrose over 4hrs
        Then 100mg/kg in 1L 5% dextrose over 16hrs
        SE: rash (tx with chlorphenamine))
      - Methionine
        
        Alternative to N-acetylcystine
        Dose= 2.5g.4hr PO for 16hrs (total 10g)
        Absorption unreliable if vomitting and lessened if concurrent activated charcoal
    - - Liver damage (ALT>1000 IU/L)
        Less than 150mg/kg - unlikely // more than 250mg/kg- likely // more than 12g total - fat
      - Paracetamol
        
        Overdose
        
        Liver conjugation becomes inundated causing paracetamol to be metabolised via alternate pathway
        Results in toxic metabolite NAPQI, itself is inactivated by glutathione
        When glutathione stores are depleted NAPQI starts to cause necrosis to liver and kidney tubules
        (Gultathione stores are built up through nourishment, therefore malnourished people have lower stores)
        Toxicity increased in patients with induced P450 e.g rifampicin, phernobarbital, phenytoin, carbemazepine, alcohol
        Other patients with lower glutathione stores: genetic variation, HIV+, malnurished, alcohol-related / liver disease
        
        Normal
        
        Reaches peak plasma concentration within an hour (or 30 mins if taken liquid or rapid absorbed form)
        Inactivated by the liver by conjugation leading to 2 metabolites: glucuronide / sulfate and excreted in urine
      - One of most common agents of intentional self harm. Can only buy 16 tablets (32 in pharmacies)
        1 tablet paracetamol= 500mg. Fatal dose= 12g or 150mg/kg (75mg/kg if malnourished)
    - - https://patient.info/doctor/paracetamol-poisoning
  - - - Always investigate aspirin, paracetamol and blood glucose
    - - Performed if suspected recreational drug use
  - - - When?
        
        Do: unconscious / unable to protect airway
        Don't: over 30-60 mins since ingestion / substance is petrol or corrosive e.g acid / bleach
      - Procedure
        
        Prepare
        
        Monitor O2 sats, prepare suction apparatus, foot of bed raised, ptx in left lateral position
        
        Perform
        
        Insert tube (ptx swallows), ensure in stomach by blowing air into tube and auscultating stomach
        Siphon stomach contents checking pH against litmus paper
        Insert 300-600ml tepid water, massage left hypochondrium
        Repeat until no new tablets siphoned
        Leave activated charcoal- 50mg in 200ml
    - - Decreases absorption in gut (50mg in 200ml water)- for paracetamol / salicylate
        Increases elimination from blood (50mg/4hr) e.g carbamazepine, dapsone, theophyllines, quinine, phenopbarbital, paraquat
        Not used for petrol, corrosives, alcohol metal salts e.g iron/lithium
        ?Not used if over 2 hours since ingestion
- - - - *Primary hyperparathyroidism in 'asymptomatic' ptx.
        Malignancy- usually associated with specific sx., typically late manifestataion of CA
        Drug causes: lithium, thiazide diuretics, vitamin D, vitamin A (rare)
- - - - Atrial Fibrilation - rate control with BB or diltiazem
        Atrial Flutter- rate control with BB
        SVT - vagal manoeuvres and adenosine
    - - Ventricular tachycardia- amiodarone infusion
        SVT with bundle branch block- treat as normal SVT
- - - - Sawtooth appearance
        Narrow complex tachycardia
        Atrial contraction up to 300bpm and ventricular contraction 150bpm (stimulated every second lap due to long refractory period of AVN)
    - - Rate/rhythm control- BB / Cardioversion
        Treat underlying cause e.g HTN / thyrotoxicosis
        Radiofrequency ablation of re-entrant rhythm
        Anticoagulation based on CHA2DS2VASc
    - - Caused by re-entrant rhythm- extra electrical pathway causing self-perpetuating electrical signal loop
        Associated conditions- HTN, ischaemic heart disease, cardiomyopathy, thyrotoxicosis
- - - - E.g Bendrofumethiazide - inhibit sodium/chloride reabsorption at DCT
        SEs: hypokalaemia, hyponatraemia, hypotension, and hyperuricaemia (can precipitate gout)
    - - E.g furosemide, bumetanide- inhibit sodium/chloride reabsorption at loop of henle
        First line diuretics for symptomatic HF
        SEs: hypokalaemia, hyponatraemia, hyoptension
    - - E.g Spironolactone
        Aldosterone antagonist- causes increased sodium excretion and reduced potassium excretion
        Regular monitoring of ptx potassium levels to detect hyperkalaemia
        SEs hyperkalaemia, hyponatraemia,hypotension gynaecomastic, menstrual disturbance
- - - - Anaplastic- rare, generally elderly people
      - Papillary >80%: *Women, slow growing, spread to lower lymph nodes
      - Follicular ~15% assoc. vascular invasion and distant mets
  - - - Amiodaraone- high iodine content and structural similarity to thyroxine.
        Monitor TFTs in someone on amiodarone
  - - - S&S: elevated temperature, abdo pain/diarrhoea, tachycardic, arrhythmia (*AF)
      - Mx: IV fluids, Oral propylthiourcacil, IV hydrocortisone, Bblockers, urgent endocrine review
      - PPh: rare. precipitated by surgery, infection, trauma, MI, DKA, radioactive iodine
      - Ix: low TSH, raised T4
  - - - Eye signs= optosis (exophthalmus), diplopia, lid lag
- - - - Addison's
        
        Mx: hydrocortisone and fludrocortisone (replace glucocorticoid and mineralocorticoid)
        patient education- including Medic-Alert and steroid card
        
        Steroid requirements- other illness, stress of surgery or pregnancy increases requirements of cortisol therefore ptx. may need parenteral steroid replacement
        
        Developed world- *AI adrenalitis
        Worldwide- TB
        
        Ix: short synthacthen test, give ACTH and if there is a lack of normal cortisol rise then this suggests adrenal failure
        
        Test results: Hyponatraemia, hyperkalaemia, eosinophila, normocytic anaemia, elevated ura
    - - Tumours of chromaffin cells of adrenal medulla, secrete catecholamines (adrenaline)
        Causes life-threatening hypertension / cardiac arrhythmias
        Mx: surgical excision and alpha blockade (phenoxybenzamine) followed by beta blockade (propanolol)
  - - - Anorexia, wt loss, N+V, dizzy/syncope,
        Can be misdiagnosed as psychiatric illness
    - - Case results: hypoglycaemia, hyponatraemic, hyperkalaemic
      - Top tip: if hyponatraemia and hyperkalaemia consider adrenal insufficientcy
      - Serum cortisol, ACTH stimulation test (synatheen test)
    - - 4Ss- sugar, steroid, saline, search for underlying cause
- - - - Depression, psychosis, thinned hair, moon face, acne, hirtuism
        Supraclavicular fat bad
        HTN, IHD, central obesity, peptic ulcer, purple striae (from wt. gain)
        Dysmenorrhoea, impotence
        Proximal myopathy, thin skin, easy bruising
      - Short stature in childhood due to glucocorticoid-induced growth arrest
        Pigmentation of skin due to high ACTH
      - *Women, 20-40yo
        Commonest cause ACTH-secreting pituitary tumour
      - Ix: 24hr UFC (urinary free cortisol), overnight dexamethasone suppression test, midnight cortisol
  - - - Ix
        
        OGTT- lack of normal suppresion of GH (glucose load in acromegaly)
        IGF-1 - long half life and elevated in acromegaly
        Calcium concentration high because GH increases alpha-hydroxylase activity or because of associated primary hyperparathyroidism
      - PPh: Pituitary adenoma which causes increased GH release
      - Mx
        
        Dopamine agonists, somatostatin agonists, GH receptor analogues, pituitary surgery,
- - - - Don't give glucagon for malnourished / alcoholics
      - Mild- able to swallow- 15-20g fast acting glucose following long acting carbs
        Moderate- conscious- 2 tubes of glucogel
        Severe- reduced GCS- 1mg Glucagon IM, IV dextrose 20%
    - - Sweating, N, confusion, anxiety, coma, seizure
      - Anyone with reduced GCS consider hypoglycaemia
      - Presentation may mimic- stroke, seizure, drug abuse, alcohol, reduced GCS
    - - Check glucose again ~10mins later
    - - Criteria: Glucose < 3mmol/L, Sx of hypo, resolution of sx with correction of hypo
        Causes: overdose insulin, increased activity, insufficient food, alcohol, infection, addinson's
      - Physiological response:
        Adrenergic- glucose metabolism- tachy, sweat, tremor, alertness
        Glucagon- gluconeogenesis, glyogenolysis
        Cortisol- increases insulin resistance
        Hunger
        Insulin- decreased production
  - - - Diagnostic crtieria:
        Metabolic acidosis (pH<7.3 or bicarb <15), Elevated ketones >3mmol/L / ketonuria +++
        Glucose- >11.1mmol/L or known DM
      - Septic screen ?infective cause- blood cultures, CXR, MSU MC&S.
        Plasma osmolality- raised in DM
    - - Specifics
        
        Insulin= If glucose >20mmol/L and delay in starting insulin infusion anticipated- 10 unit IM bolus soluble insulin
        Infusion 50 units soluble insulin in 50ml NaCl 0.9% solution (0.1 units/kg/hr)
        
        Fluids: 1L NaCl bolus, 1L over 1 hr, 1L over next 2-4hrs, 1L over next 4-6hrs thereafter
        
        Magnesium= Mg deficiency (recognised comp of DKA) to be corrected- not doing causes fitting/ arrhythmia
      - General
        
        Practicalities= large bore cannula in 2 sites, 1 cannula for insulin.
        Follow trust protocol...principles of management:
        IV fluids 0.9% NaCl with KCl , 10% dextrose when glucose <14mmol/L, IV insulin 0.1units/kg/hr
      - Monitoring
        
        U&E- ?hypokalaemia caused by insulin infusion
        Glucose- ?hypoglycaemia- when glucose <14mmol/L add 10% decxtrose
        Ketones- continue insulin infusion until ketones are <0.06mmol/L
        Persistent acidosis or hyperkalaemia, or if ptx becoming fluid overloaded - dialysis
    - - First presentation T1DM, silent MI, ischaemic bowel, stroke, infection, medication
    - - IV access can be poor, cerebreal oedema- rapidly correcting fluids can cause CO,
        Marked hypokalaemia caused by insulin infusion
        Top tip: if someone has metabolic acidosis check their ketones - DM, alcoholism, starvation
    - - Polydipsia, polyuria, dehydration, abdo pain, vomiting, anorexia, fatigue,
- - - - Hypercalcaemia
        
        Mx: IV fluids ~3L 24hr, bisphosphonates
        
        Ix: serum calcium, PTH
        
        S&S: bones, stones, moans, psychiatric groans
        
        PPh: hyperparathyroidism, malignancy
      - Hyperparathyroidism
        
        Primary
        
        PPh: benign adenoma produces excess PTH
        S&S: bones, stones, abdominal groans, psychic moans,
        Ix: Bloods=PTH raised, Ca2+ raised, Urine= increased Ca2+. Imaging= DEXA- bone resorption, US kidney- stones. Biopsy= ?CA
        Mx: Increase Vit D, high fluid intake, bisphosphonates, HRT, ?surgery
        
        Secondary
        
        PPh: ptx with CKD have chronic hypocalcaemia --> parathyroid hyperplasia
        S&S: (of hypocalcaemia) muscle cramps, paraesthesia, seizure, coma, ostemalacia from vit D deficiency
        Ix: low calcium, raised PTH
        Mx: calcium supplements, correct vitamin D deficiency, surgery
        
        Tertiary
        
        PPh: following prolonges 2nd hyperparathyroidism, parathyroid glands become autonomous and produce excess PTH even after hypocalcaemia is corrected
        S&S: bones, stones, abdominal groans, psychic moans
        Ix: raised ca2+, raised PTH
        Mx: surgery
      - Other Causes
        
        Bone mets, tumours which secrete ectopic PTH,
        Granlomatous diseases e.g sarcoidosis/TB--> lymph nodes full of macrophages- macrophages convert vit D to 1,25 vit D.
        Thiazide-like diuretics
    - - PPh: corrected calcium= total serum calcium + (0,02 x (40-serum albumin))
        Causes= Vit D deficiency, hypoparathyroidism (di george syndrome), pseudophyoparathyroidism (resistance to PTH) surgery, AI, magnesium deficiency
        S&S: paraesthesia, muscle spasms, seizures, coma. long QT, cataracts. Chovostek's sign (tapping facial nerve causes twitch), Trousseau's sign (BP cuff >20mmhg systolic >5mins causes wrist flexion)
  - - - Causes
        
        Excess water, salt deficiency, pseudohyponatraemia, solute, sickle cell anaemia, SIADH, addisons
        Drugs: omeprazole, sertraline, sodium valproate
      - Classifying
        
        "Acute" hyponatraemia= <48hrs. Mild=130-135, Mod=125-130, Severe<125
      - Sx: mild confusion, coma, pseudobulbar palsy, pastic paraparesis
      - Ix: check their volaemic status, check TFT and cortisol, what drugs are they on
      - Mx
        
        Overcorrection can cause pontine myelonosis
        
        Mx of severe actue hyponatraemia:
        IV infusion 150ml 3% hypertonic saline over 20 mins,
        Check Na+ --> if Na+ increases 10mmol / goes >130 overall then stop
        Repeat
        Check Na+
      - Further Info- Repeat Intro to Endocrine Lecture