Exam Revision 3rd Year

Guillain-Barre Syndrome
(definiton + pathogenesis + causes + signs + treatment)

Rapidly progressing, acute demyelinating disorder affecting peripheral motor axons

Pathogenesis: humoral and T-cell mediated immune response and macrophage activation which attacks schwann cells and engulfs myeline sheath, causing segmental degeneraion

Causes: Campylobacter infection, CMV, EBV, HIV, prior vaccinations

Signs:

• Weakness and paralysis starting in distal limbs

• Advances proximally

Treatment:

• Paramapharesis

• IV immunoglobulins and steroid therapy

Diabetic neuropathy
(pathogenesis + signs + complications)

Pathogenesis: metabolic and ischaemic damage to nerves due to thickening of endoneurial arterioles from diabetes

Signs:

• Distal, symmetrical polyneuropathy: numbness, loss of pain sensation

• Autonomic neuropathy: disturbances in bladder and bowel function

Complications: can lead to infection and amputation

Amyotrophic lateral sclerosis (ALS)

(definiton + pathogenesis + signs + clinical progression)

Progressive neurological disorder causing selective degeneration of motor neurons responsible for voluntary muscle activity

Pathogenesis:

• Poorly understood, related to superoxide dimutase (SOD1) mutations on chromosome 21 causing neural inclusions and cytotoxicity

• LMN disease: atrophy of ventral spinal nerve roots causing skeletal muscle denervation

• UMN Disease: degeneration of corticospinal tracts in lateral portion of SC

Signs:

• LMN disease: weakness, fasciculations

• UMN disease: paresis, hyperreflexia, spasticity, +ve babinski sign

Clinical progression:

• Increasing muscle weakness and decrease in muscle bulk

• Difficulty in deglutition and speaking

• Recurrrent chst infection (main cause of death)

Diffuse axonal injury (pathogenesis + morphology + signs)

Pathogenesis: sudden severe deceleration of the brain causing disruption or shearing of axons

Morphology:

• Macroscopic: brain oedema, splinter haemorrhages

• Microscopic: retraction balls

Signs:

• Immediate coma following injury

• Signs of raised ICP (headache, confusion, nausea, papiledema)

Traumatic vascular injury (epidural, subdural, subarachnoid)
(pathogenesis + signs + CT + treatment)

Pathogenesis:

• Epidural haematoma: tearing of middle meningeal arterty following fracture of temporal bone, where arterial pressure forms rapidly expanding haematoma

• Subdural haematoma: rupture of bridging veins (usually in elderly patients with cerebral atrophy)

• Subarachnoid haematoma: injury to BV (e.g. burst aneurysm) in subarachnoid space

Diagnosis - signs:

• Epidural haemtoma: coma hours after injury

• Subdural haematoma: coma days after injury

• Signs of raised ICP

Diagnosis - CT:

• Epidural haemorrhage: hyperdense biconvex mass stopping at suture line, midline hift and ventricular compression

• Subdural haemorrhage: hyperdense/ isodense sick shape over cerebal convexity, midline shift and ventricular compression

• Subarachnoid haemorrhage: star-shapped appearance around circle of willis; severe ‘thunderclap’ headache

Treatment:

1. Treatment of primary brain/ SC injury

2. Treatment and prevention of secondary injuries e.g. phenytoin (seizure prophylaxis)

3. Monitor clinical progression: debdridement of skull fractures, evacuation of haematoma

Types of brain herniations (definition + signs)

Subfalcine herniation: displacement of cingulate gyrus under falx cerebri

Transtentorial herniation: herniation of uncus of medial temporal lobe through tentorial notch, causing pressure on rostral midbrain

Signs:

• Ipsilateral dilated and unresponsive pupil

• Contralateral hemiparesis

  • Kernohan’s phenomenon: ipsilateral hemiparesis

• Decreases consciousness or coma

• Signs of raised ICP

Tonsilar herniation: herniation of inferior medial aspects of cerebellum through foramen magnum

• Can cause compression of medulla causing cardiac/ respiratory depression and death

Glioblastoma
(definition + signs + diagnosis)

Grade IV astrocytoma

Signs of brain tumours

• Seizures

• Worsening vision

• Sensory and motor abnormality

• Headache

• Stroke-like symptoms

Diagnosis

• CT shows ring-like contrast enhancement aginst central necrosis

• Biopsy shows pleomorphism, high cellularity and infiltration of tumour cells, palisaded necrosis and microvascular proliferation

Meningioma
(defintion + diangosis)

Benign, non-infiltrating tumour frmed by extra-axial meningothelial cells

Diagnosis:

• CT shows dura-based, well-circumsised mass which does not invade underyling brain

• Biopsy: meningothelial cells show whorled appearance with psamomma bodies

Brain abscess
(definition + signs + treatment)

infection of the brain causing necrosis and abscess formation

Signs:

• Fever

• Headache

• Change in mental state

• Focal neurological deficits

• Seizures

• Nausea and vomiting

• Neck stiffness

Treatment:

• Surgical drainage of abscess

• Antiobiotic therapy

• Elimination of primary site of infection

Ischaemic stroke (focal)
(definiton + causes + diagnosis + treatment)

Obstruction of blood supply to a localised area of the brain for a long enough period of time

Causes:

• Embolic (20%): from heart, aorta and carotid arteries, paradoxical emboli

• Thrombosis (80%): usually non-haemorrhagic

Diagnosis:

• Signs: FAST

• CT appaears hypodense on side of lesion

Treatment:

1. Stabilisation: maintain airways (ventilator, endotracheal tube, O2, monitor glucose, BP, hydration)

2. If ischaemic <8 hours: alteplase + mechanical thrombectomy

   1. <9 hours if surviving penumbra, <4.5 hours if no surviving penumbra

3. Aspirin/ clopidogrel after 24hrs of alteplase administration

4. Management of comorbidities (e.g. AF, MI, HTN, diabetes)

5. Physiotherapy, OT, speech therapy

Alzheimer’s disease
(signs + pathogenesis)

Signs:

• Short-term memory loss

• Impairment of visuospatial skills

• Disorientation, word-finding difficulty

• Ultmate loss of mobility and speech

• Diffuse cerebral atrophy

• Biopsy shows NFT’s and neuritic plaques

Pathogenesis: extrcellular deposition of AB peptides which aggregate to form amyloid fibrils. These cause neuronal injury and dysfunction, and stimulate an inflammatory response causing neuronal damage and phosphorylation → aggregation of tau proteins

• Sporadic, late-onset AD: ApoE gene on chr 19

• FAD: APP, PSEN1/PSEN2 gene

Huntington’s disease
(defintion + pathogenesis + age of onset + signs)

Progressive and fatal autosomal dominant disease clinically characterised by progressive movement disorder and dementia

Pathogenesis: mutation on HD gene of chr4 which normally encodes for huntingtin protein, resulting in >40 CAG repeats. This causes formation of intraneuronal inclusions on huntingtin protein

Age of onset: 25-45 yrs

Signs:

• Signs of dementia

• Chorea

• Macroscopic morphology shows atrophy of caudate and compensatory dilation of ventricles

Creutzfeld-Jakob disease
(definiton + pathogenesis + source of infection + signs)

Infectious prion disease causing rapid onset of fatal dementia

Pathogenesis:

1. Spontaneous conformational change from normal to abnormal prion protein

2. Prions bind to other normal prions which progressively reproduc and form aggregates

Sources of infection:

• Contaminated corneal transplants

• Dura mater grafts

• Human growth hormone

Signs:

• Onset 50-75 yrs

• Rapidly progressing dementia with myoclonus

• Biopsy shows spongiform transformation of cortex

Post-streptococcal GN
(definition + pathogenesis + diagnosis)

Glomerulonephritis with nephritic syndrome appearing 1-4 weeks following skin/ pharyngeal infection from GAS

Pathogenesis:

1. Host immune response to pathogenic antigen causes immune complex deposition in a subendothelial location (which migrates to subepithelial)

2. Subsequent complement activation and inflammation causes proliferation of endothelial and mesangial cells

Diagnosis:

• Fever, malaise, nausea

• Nephritic syndrome: oliguria, haematuria, mild proteinuria, mild-moderate HTN

• Elevated tiers of anti-streptococcal Ab’s and low serum C3

• Periorbital oedema

• Urinalysis shows red cell casts

• Biopsy shows enlarged, hypercellular glomerulus with subepithelial immune complex deposit, granular immunofluorescence

Membranous nephropathy
(definiton + pathogenesis + diagnosis + treatment)

Glomerulonephritis with nephrotic syndrome

Pathogenesis:

1. 75% of cases HLA-related autoimmune

2. Accumulation of IgG-containing immune complex deposits in subepithelial location. These become incorporated into the GBM causing thickening

3. Activation of complement cascade including C5-C9 MAC. This releases proteolytic enzymes which damage foot processes causing proteinuria

4. NO inflammatory cells recruited as C3a + C5a not on capillary side of BM (cannot travel)

Diagnosis:

• Nephrotic syndrome: heavy proteinuria, hypoalbuminemia, generalised oedema, hyperlipidemia and lipiduria

• Biposy of kidney shows thickened GBM, spiked appearance, no inflammatory cells, granular immunoflurosence

Treatment:

• Frusemide (oedema)

• ARB/ACE-I (reduce proteinuria by ↓ GFR)

• SGLT2-I (reduce proteinuria by ↓ GFR)

Gout
(definiton + pathogenesis + diagnosis + treatment)

Accumulation of sodium-urae crystals within joints

Pathogenesis: Hyperuricaemia causing deposition of monosodium-urate crystals in the joints. Flare ups caused by immune response to urate crystals

Genes involved: SLC2A9 (for GLUT2 receptors), IL-37

Diagnosis:

• Sudden onset of excruciating pain within the joint (often metatarsophalangeal)

  • Advanced gout: recurrent flare with persistent joint pain

• Gold standard: presence of MSU crustals in synovial fluid taken from joint aspiration during flare

• Serum urate >0.42mmol/L

• Imaging via x-ray, ultrasound, CT shows urate crystals

Treatment:

• Colchicine or NSAID’s (reduces inflammation)

• Low dose allopurinol (lowers urate levels)

• Ice (pain relief)

• Lifestyle: limit alcohol, purines, sugar intake, weight loss in obese

Acromegaly
(definiton + signs + investigations + treatment)

Excess of GH, most often caused by secretory adenoma of somatotroph cells

Signs:

• Prepuberty: extreme height (gigantism)

• Postpuberty: growth of hands, feet, lower jaw (gaps between teeth), lips, nose

• Cardiovascular disorders

• Impaired glucose tolerance (diabetes)

Investigations:

• High GH, high IGF-1, loss of diurnal GH pattern

• Elevated glucose

Treatment:

• Transphenoidal surgery and radiation (remove tumour)

• Octreotide (somatostatin analogue)

Hyperprolactinemia
(defintion + signs + treatment)

Excess prolactin secretion, usually caused by prolactin secreting tumour, or drugs that reduce dopamine levels and transmission (e.g. antipsychotics)

Signs:

• Women: cessation of periods, inappropriate lactation (galactorrhea)

• Men: gynacomastia

Treatment:

• In psychotic patients, alternative medications

• Tumour: surgical removal

Hyperthyroidism (grave’s + toxic nodular disease + 1/2 hyperthyroidism)

(definiton + signs + treatment)

Grave’s disease: autoimmune condition causing anti-thyroid peroxidase Ab’s to stimulate TSH receptors

Toxic nodular disease: autonomous benign nodules which slowly increase thyroid production

Primary/ secondary hyperthyroidism: TSH or T4-producing adenoma

Signs:

• Heat intolerance, weight loss, increased appetite, muscle weakness, diarrhoea, difficulty sleeping, anxiety

• Grave’s: exopthalmos, goitre, High T3/T4, low TSH, diffuse uptake of radioactive iodine

• Toxic nodular disease: nodular uptake of radioactive iodine

Treatment: carbimazole, surgical removal of thyroid gland, radioactive iodine, symptomatic relief (e.g. beta-blockers)

Cushing’s syndrome (cushing’s disease, ectopic tumour, adrenocrotical tumour)

Cushing’s disease: pituitary adenoma causing ACTH secretion

Ectopic tumour: ectopic tumour elsewhere in body secreting ACTH

Adrenocortical tumour: tumour in adrenal cortex secreting cortisol

Diagnosis:

• Signs: central adiposity, moon face, oesteoporosis, poor wound healing and infections, stretch marks, low mood, hyperglycaemia, hypokalaemia, HTN

• Cushing’s disease (pituitary adenoma): high cortisol, high ACTH, partial response to high dose DST, IPSS shows high ACTH

• Ectopic tumour: high cortisol, high ACTH, no response to high dose DST

• Adrenocortical tumour: high cortisol, low ACTH

Treatment:

• Ketoconazole or metrapyrone

• Withdraw glucocorticoid therapy if drug-induced

Addison’s disease (adrenal insufficiency)
(definition + diagnosis + treatment)

Autoimmune disease causing destruction of adrenal tissue

Diagnosis:

• Signs: fatigue, aching, dizziness, weight loss, hypoglycaemia, hyperkalaemia, dark skin, dehydration, hypotension

• Low cortisol, low aldosterone, high ACTH

Treatment: glucocorticoid replacement e.g. prednisone

Phaeochromocytoma
(definition + diagnosis + treatment)

Tumour of adrenal medulla causing hypersecretion of adrenaline and NA

Diagnosis:

• Signs: episodic panic attacks, tachycardia, sweating, anxiety, HTN

• High HMMA/ VMA (metabolites of catecholamines in urine)

Treatment:

• Phenoxybenzamine (alpha adrenergic blocker)

• Symptomatic relief: beta-blockers

Congenital adrenal hyperplasia
(definition + diagnosis + treatment)

Deficiency in 21-hydroxylase enzyme, prventing synthesis of hormones in the adrenal glands

Diagnosis:

• Signs: polyuria, thirst, hypotension, stress, low BGC between meals, failure to thrive, precocious puberty

• Low/ normal cortisol and aldosterone

• High 17-OH-progesterone

Treatment:

• Glucocorticoid replacement (cortisol): prednisone

• Mineralocorticoid replacement (aldosterone): fludrocortisone

Acute lymphoblastic leukaemia

(definition + pathogenesis + diagnosis + treatment + prognosis)

Most common cancer in children, causing rapid proliferation of pre-B lymphoblasts in bone marrow

Pathogenesis: numerical or structural chromosomal changes causing bone marrow to be packed with rapidly dividing pre-B lymphoblasts which fail to mature

Diagnosis:

• Anaemia, neutropenia, thrombocytopenia (pancytopenia)

• Bone pain

• Lymphadenopathy, splenomegaly, hepatomegaly

• Blood film and biopsy: circulating lymphoblasts

• Immunohistochemistry: TdT, CD10, CD19, CD20

Treatment: invasive chemotherapy followed by consolidation and maintenance

Prognosis: if hyperdiploidy (>50 chromosomes/ cell) - good prognosis

Follicular lymphoma
(defintion + pathogenesis + diagnosis + treatment + prognosis)

Low grade B-cell NHL causing B-cell lymphocytes to be arranged in follicular pattern in LN’s. Commonly affects >50yrs

Pathogenesis: translocation of BCL2 gene on chr 18 with IgH gene on ch 14, causing overexpression on BCL2 gene which inhibits apoptosis. This forms a clone of mature B cells which fail to die by apoptosis, resulting in geriatric overcrowding

Diagnosis:

• Signs non-contiguous lymphadenopathy, fever, night sweats, weight loss

• CD19 & CD20 positive immunohistochemistry

Treatment: Chemotherapy and/ or immunotherapy (e.g.rituximab)

Prognosis: not curable, survival 7-9 years

Hodgkin lymphoma
(definition + diagnosis + treatment + prognosis)

Neoplasms characterised by Reed-Steenberg cells

Diagnosis

• High risk: young adults with EBV infection

• Signs of contiguous lympadenopathy, weight loss, fever, night sweats

• Blood film: Reed-steenberg cell surrounded by reactive cells

Treatment: systemic chemotherapy, sometimes with field radiotherapy

Prognosis: 5-year survival close to 100%

Hypercalcaemia (primary hyperparathyroidism, hypercalcaemia of malignancy, multiple myeloma, metabolic acidosis)

(definition + signs + treatment)

Primary hyperparathyroidism: parathyroid adenoma causing autonomous production of ACTH

• Investigations: high Ca2+, low PO4, high PTH, high ALP

Hypercalcaemia of malignancy: tumour (e.g. SCC) secretes PTHrP

• Investigations: high Ca2+ (high ALP, low PO4), low PTH,

Multiple myeloma: metastasis of bone cancer causing bone breakdown

• Investigations: high Ca2+, high PO4, -ALP,

Metabolic acidosis: high H+ causes increase in ionised Ca2+

• Investigations: high ionised Ca2+, -total Ca2+

Signs:

• Fatigue

• Weakness

• Polyuria/ nocturia

• Dehydration

• Constipation

• Nausea

• Renal stones

• Low mood

• HTN

• Bone disorders

• CKD (from chronic high Ca2+)

Treatment:

• Restore circulating volume

• Parathyroidectomy (if hyper)

• Bisphosphonates (_onate)

• Calcitonin

• Frusemide

• Prednisone

Hypocalcaemia (vitamin D deficiency, hypoparathyroidism, metabolic alkalosis, renal failure, pseudohypoparathyroidism)

(definition + invesitgations + signs + treatment)

Vitamin D deficiency/ malabsorption: lack of vitamin D and thus calcitriol, prevent Ca2+ absorption from the gut

• Investigations: Low Ca2+, low PO4, high PTH, high ALP

Hypoparathyroidism: lack of PTH (e.g. parathyroidiectomy)

• Low Ca2+, low PTH

Metabolic alkalosis: low H+ which reduces ionised Ca2+ levels

• Investigations: Low ionised Ca2+, normla total Ca2+,

Renal failure: inability to reabsorb Ca2+, and excrete PO4, creatine, urea

• Investigations: low Ca2+, high PO4, high creatine and urea

Psuedohypoparathyroidism: end organ resistance to PTH

• High PTH, low Ca2+, high phosphate, -ALP

Signs:

• Pins and needles

• Tetany/ convulsions

• Numbness/ parasthesia

• Stridor

• Cataracts

• Psychological disturbances

• +ve Chvostek and Trousseau’s signs (face twitching upon tapping)

Treatment:

• cholecalciferol, calcitriol

• Thiazides

Chlamydia (definiton + complications + signs + diagnosis + treatment)

STI caused by chlamydia trachomatis

Complications (F): pelvic inflammatory disease causing infertility and ectopic pregnancy

Signs (mostly asymptomatic):

• Painful ejaculation (M) and intercourse

• Clear, mucoid penila/ vaginal discharge

• Testicular swelling (F)

• Bleeding between periods (M)

Diagnosis:

• Nucleic acid amplification test (NAAT)

• Culture of first pass urine samples or swabs: gram -ve, ovoid shape

Treatment:

• Azithromycin 1g once OR

• Doxycycline 100mg orally 2/ day for 7 days

Gonorrhea (definition + complications + signs + diagnosis + treatment)

STI caused by Neisseria gonorrhoeae

Complications (F): PID, infertility, neonatal infections

Signs:

• Heavy yellow/white/ green purulent discharge

• Burning sensation while urinating

• Painful/ swollen testicles or vulva

• Swollen glands/ burning in throat

• Bleeding between periods or after intercourse

• Conjuctivitis (neonates as well)

Diagnosis:

• Microscopy and culture of swabs from pus secretions: intracellular gram-ve diplococci and oxidase +ve

Treatment: ceftriaxone 250mg and azithromycin 1g

Syphilis
(definiton + complications + symptoms + diagnosis + treatment)

STI caused by treponema pallidum

Complications:

• Can progress to 2˚ syphilis causing condylomata lata (flat, wart-like lesions)

• Late stage syphilis fatal if untreated

Symptoms:

• Appear 2 weeks after infection

• Chancre’s: small lesions on genitalia without inflammation

• 2˚ syphlis: disseminate to rest of the body 5-8 weeks after initial symptoms resolve

• Late stage syphilis: insanity and death

Diagnosis:

• Serology of blood sample using EIA, later confirmed by rapid plasma receptor antigens (RPR) or TPPA (T. pallidum plasma agglutination)

• Swab of ulcer for T. pallidum (specialist only)

Treatment: benzathine penicilin (all stages)

Epilepsy + status epilepticus
(defintion + diagnosis + treatment)

Epilepsy = tendency to have convulsions/ transient abnormal events resulting from paroxysmal discharge of cerebral neurons

Diagnosis:

• 2 or more unprovoked seizures more than 24 hrs apart

• Risk of another seizure after 1 unprovoked seizure the same as after 2 unprovoked seizure

• In reflex epilepsy, at least 2 seizures in response to event (e.g. strobe lights)

• Signs: focal or generalised involvement of the brain, impaired awareness and/ or motor involvement (depends on type of seizure)

  • Tonic clonic: generalised, impaired awareness with tense muscles and clonus

  • Absence seizures: focal with brief lack of response

• EEG shows sudden sustained and rhythmic firing

Treatment:

• Antiepileptic drugs (e.g. phenytoin, valproate, levetriacetam)

• Vagal nerve stimulation (extreme cases)

Status epilepticus: medical emergency when seizure lasts >5 minutes or without rcovery period in between 2 seizures

• Treatment: benzodiazepines, AED’s, intubation and ICU

Chronic kidney disease
(definition + causes + signs + treatment)

Any decrease in kidney function over a minimum of 3 months (typically eGFR <90ml/ min)

Causes:

• HTN: sustained high intragllomerular P → thickening of renal a’s → ischaemic injury and sclerosis of glomeruli → decreased filtration

• Diabetes: high BGC causing non-enzymatic glycation of BV's → hyaline arteriosclerosis of efferent arteriole → raised intraglomerular P → sclerosis of kidney → decreased filtration

• CVD, smoking, age, obesity

Signs:

• HIgh urea and creatinine

• Hyperkalaemia (→ arrhythmia)

• Hypocalcaemia (less conversion of vit D to calcitriol → PTH release → bone resoprtion of calcium → renal osteodystrophy)

• HTN (decreased filtration → renin release → Na+ and water reasorption)

• Anaemia (lack of EPO production)

• Metabolic acidosis (lack of HCO3- production)

Treatment:

• Treat underlying cause (e.g. ACE-I’s for HTN)

• CVD risk management: b-blocker, SGLT2i, weight control, lipid lowering therapies

• If oedema: frusemide

• Dialysis or kidney transplant

• EPO, calcitriol supplementation

Hypoglycaemia
(definiton + signs + treatment)

Glucose <4mmol/L (<3.1 in moderate, <2.2 in severe)

Signs:

• Trembling

• Intense hunger

• Sweating

• ↑HR

• Weakness

• Confusion

• Seizures/ coma

Treatment: medical emergency

• Mild-moderate: oral glucose (15g candy or 200ml orange juice)

• Severe: IM or SC glucagon

Type 1 diabetes mellitus (definition + signs + diagnosis + complications + management)

Autoimmune destruction of pancreatic beta cells, causing impaired insulin production

Signs

• Polyuria

• Excessive thirst (polydipsia)

• Frequent urination

• Severe: nail polish breath (keotacidosis)

Diagnosis: lab findings on 2 separate occasions, with appropraite signs and symptoms

• Fasting BGC >7mmol/L, random BGC >11.1mmol/L

• Glucose in urine

• HbA1c >50mmol/L

Complications: muscle atrophy, ketoacidosis, diabetic retinopathy, diabetic neuropathy,

Management:

• Insulin glargine + aspart: basal-bolus regimen (or insulin pump)

• Glucose monitoring

• Oral glucose available (in case of hypoglycaemia)

Type 2 diabetes mellitus
(definition + risk factors + complications + management)

impaired insulin secretion and insulin resistanc,e usually from result of prolonged elevated glucose

Risk factors

• Adult onset

• FH (polygenic disorder)

• Obesity

• Dyslipidaemia

• HTN

Complications:

• Cardiovascular disease (atherosclerosis causing ischaemia)

• Diabetic retinopathy and neuropathy

• Peripheal neruopathy causing infection and gangrene

• Diabetic nephropathy

• Cataracts

Management:

• Dietary intervention and physical exercise

• Metformin, empagliflozin, dulaglutide

• Insulin if uncontrolled

Acute kidney injury (definition + causes + diagnosis + management)

Any abrupt decline in renal function within 48 hours, defined as

• Increase in serum creatinine >27umol/L within 48 hrs or >50% over 7 days

• Oliguria <0.5ml/ kg/ hour

Causes

• Low perfusion (volume depletion, ventricular failure, vasodilation)

• Inflammatory (e.g. GN)

• Obstructive

• Nephrotoxic

Diagnosis

• ↓ GFR

• Oliguria

• Metabolic acidosis with respriatory compensation

• Hyperkalaemia → arrhythmia

Management

• Correct underlying cause of AKI (e.g. N-saline if volume depletion)

• Correct complications of AKI (e.g. NaHCO3 formetabolic acidosis)

• AVOID giving ACE-I/ARB initially (will ↓GFR)

• CVS + CKD protection - long-term

Herpex simplex encephalopathy

Complication of HSV infection causing encephalitis

Pathogenesis:

1. Viral transmission onto epithelial cells (mouth/ lips)

2. Retrograde transport via CN I or V

3. Remains latent in nucleus

4. Reactivation via anterograde transport

5. Transmission to temporal lobe causing inflammation
   

Diagnosis:

• Signs: headache, fever, psychiatric symptoms, seizures, altering LoC

• MRI shows inflammation of temporal lobe

• CSF: DNA amplifcation of virus, moderate WBC and proteins
  

Complications: cerebral venous sinus thrombosis

Treatment: acyclovir