Miscellaneous Flashcards
What is a granuloma?
A collection of macrophages (as few as 4).
They often fuse and form Giant Cells
What is a non-caseating granuloma?
A non necrotising granuloma
What causes hereditary and acquired angioedema?
Caused by a deficiency or dysfunction of the C1 inhibitor.
This results in increased levels of bradykinin because C1 inhibits activated kallikren (required for the generation of bradykinin) in the kinin system pathway.
C1 inhibitor is a protein that regulates the classical complement pathway.
Explain about Hereditary Angioedema
Autosomal Dominant
2 types:
1= 80% inadequate C1-inhibitor production
2= production of dysfunctional C1-inhibitor
C1 inhibitor functional tests are abnormal in both, in type 2 C1 inhibitor levels are normal.
Kinins generated secondary to complement activation play a role in vascular leakage contributing to angio-odema.
usually presents during childhood or adolescence.
Explain about Acquired Angioedema
C1-inhibitor may be excessively consumed by : clonal B lymphocyte proliferation ( B-cell lymphoma) or massive immune complex type disease.
May also be caused by autoantibodies that block or interfere with otherwise normal C1-inhibitor function.
Distinguished from HAE by late adult onset, non-familial and with reduced levels of C1q
What are the triggers for Hereditary and Acquired Angioedema?
Injury/infection surgery/dental treatment stress pregnancy certain medications like the contraceptive pill
What are the symptoms for Hereditary and Acquired Angioedema?
Non-pruitic, recurrent, angio-oedematous swellings.
Common sites being- lips, tongue.eyelids,larynx and GI tract
Manifestations that suggest intestinal obstruction include N&V and colicky discomfort/
Bronchospasms don’t occur but laryngeal oedema may be present causing stridor.
What is the aetiology of Idiopathic Intracranial Hypertension?
Unknown
Highly associated with females and obesity (esp recent weight gain)
What is the pathophysiology of Idiopathic Intracranial Hypertension?
CSF absorption occurs both via the arachnoid granulations and along nerve root sheaths, especially along the olfactory nerve (cribform plate)
Thought that there is an increase in resistance to CSF outflow along one or both pathways.
What is the characteristic of Idiopathic Intracranial Hypertension?
Raised Intracranial Pressure in an alert, orientated patient without localising neurological findings or an obvious cause
What are the clinical features of Idiopathic Intracranial Hypertension?
Headache= severe, pulsatile, daily and may awaken pt.
Nausea Common
Neck and Shoulder Pain
Transient Visula Obscurations= episodes of transient grey/brown outs that last <30secs. they can be mono or bi-ocular. Thought to be transient ischaemia of the optic nerve.
Pulse-synchronous Tinnitus= 60% patients. Specific. Sound is often unilateral- jugular pressure ipsilateral to the sound abolishes it.
How do you manage Idiopathic Intracranial Hypertension?
1) Elimination of causal factors = weightloss
2) Acetazolamide (except 1st trimester of pregnancy)
+ Persistant headache= naproxene or amitriptyline or CSF shunting
+ Progressive visual loss= optic nerve sheath fenestration or CSF shunting
What is Cushing’s Reflex?
Bradycardia, Systolic Hypertension and Cheyne-Stoke respiration (irregular)
How does Cushing’s reflex occur?
In response to raised intracranial pressure
Causes+ primary/met tumour, head injury, haemorrhage, infection, hydrocephalus,cerebral oedema, status epilepticus.
Can also get if LP performed when there is a raised intracranial pressure ( except in IIH)
can also result from a low cerebral perfusion pressure (<15mmHg)
Mechanism of action of Cushing’s reflex?
1) ICP>MAB therefore get cerebral arteriole compression=cerebral ischaemia. In response to ischaemia you get sympathetic stimulation of arteries= constrict. This increases total resistance and increases MAB to try and restore bloodflow to the brain. Increase HR and CO
TACHYCARDIA AND HYPERTENSION
2) Baroreceptors in aortic arch detect raised BP and trigger parasympathetic response via vagus nerve (ICP may also distort vagus nerve and directly stimulate this pathway).
This induces BRADYCARDIA
3) Raised ICP causes increased pressure on the brain stem. Changes homeostasis and causes irregular breathing patterns.
What is a hernia?
The protrusion of a viscus into an abnormal space
What is a direct inguinal hernia?
Caused by a weakness in posterior wall of the inguinal canal.
Abdo contents forced through defect and into the canal
Hernia emerges medial to the deep ring canal (mid-point between ASIS and PT)
What is an indirect hernia?
Does not pierce posterior wall of the canal. The contents pass through the deep ring and exit via the superficial ring.
If you reduce the hernia and then press on the deep ring and get the patient to cough the hernia doesn’t re-emerge.
What is a femoral hernia?
The abdominal contents pass inferior to the inguinal canal and emerge in the femoral canal ( within the femoral sheath, medial to the artery and vein)
Space is tight and it is bordered medially by the edge of the lacunar ligament.
Increased risk of obstruction and strangulation.
How to you calculate maintenance fluid for children?
1st 10kg = 4ml/kg/hr or 100ml/kg
2nd 10kg = 2ml/kg/hr or 50ml/kg
all other kg= 1ml/kg/hr or 25ml/kg
+ ongoing losses
measured and replaced 4hrly
What is normal urine output for a child?
1ml/kg/hr
what is normal urine output for an adult?
0.5ml/kg/hr
What is an ALTE?
Apparent Life Threatening Event.
Apnoea that lasts over 30 seconds
What are the causes of Apnoea?
1/3 unknown
1/3 GORD
1/3 Other= RSV (prem), seizure, sepsis, pertusiis, sub-dural ( shaken baby)
Normal stop after 6 months. If they haven’t consider epilepsy or NAI
FEVER UNDER 5
Herpes Simplex encephalitis
Focal Neurological Symptoms
Focal Seizures
Reduced consciousness
FEVER UNDER 5
Kawasaki Disease
fever longer than 5 days + 4/5 features
Bilateral Conjunctival Injection
Change in Mucus Membrane in upper respiratory tract (inflammed pharynx, dry cracked lips, strawberry tongue)
Change in extremeties (oedema, erythema, desquamination)
Polymorphous Rash
Cervical Lymphadenopathy
FEVER UNDER 5
Meningicoccal Disease
Fever Non Blanching Rash lesions larger than 2mm in diameter (purpura) cap refil >3 seconds neck stiffness
Meningitis
Bulging fontanelle
reduced conciousness
convulsive status epilepticus
FEVER UNDER 5
Pneumonia
Tachypnoeic (RR 0-5 months 60mins, 6-12 months >50mins, >12months >40/min)
Crackles in chest
Increase in WOB- nasal flaring, chest indrawing
Cyanosis
<95% O2 sats on air
FEVER UNDER 5
Septic Arthritis/ Osteomyelitis
Swelling of limb/joint
Not using an extremity
Non-weight
FEVER UNDER 5
Urinary Tract Infection
Any fever <3 months
>3months fever + 1
vomiting, poor feeding, lethargy, irritability, abdo pain/tenderness, urinary frequency/dysuria
What are the classifications of generalised seizures?
1) TONIC CLONIC (Grand Mal)
2) Generalised Tonic
3) Generalised Clonic
4) Absent Seizures (Petit Mal)
5) Myotonic seizure (one ,or multiple, muscle groups involved)
6) Atonic ( total loss of muscle tone)
Describe Tonic Clonic Seizures
1) often preceding aura
2) TONIC- ictal cry (laryngeal spasm), cyanosis ( reduced resp) and contraction of the jaw. Sympathetic over-drive (tachycardic etc). Usually transient lasts a few seconds.
3) CLONIC- alternating and rapid muscle contraction and relaxation. Can last upwards of a few minutes
4) post ictal= confusion and reduced consciousness that can last a few hours.
What are simple partial seizures?
Concious level is not impaired isolated sensory/motor features head turning may have no objective signs Todd's paresis may be apparent (weakness post limb seizure)
What are complex partial seizures?
Impairment of concious level temporal lobe- ja maid vu or deja vu, lip smacking Frontal cortex- autonomic disturbance Parietal- sensory disturbance Occipital cortex- visual disturbance
Can progressto secondary generalised seizure of there is involvement of limb/muscle group that spreads- Jacksonian Arch
What is Status Epilepticus?
A seizure lasting >5mins or repeated seizures w/out regaining consciousness.
MEDICAL EMERGENCY
How do you treat Status Epilepticus?
1) ABCDE
2) Lorazepan 4mg IV or 10mg Diazepam PR
3) identify and reverse any underlying cause
4) if contine longer than >30min = phenytoin infusion (15mg/kg @ 50mg/min) and an anaethetist for GA and ITU admission
Tx of Anaphylaxis?
ABCDE Adrenaline IM Adults 500 micrograms of 1:1000 Children >12 500 micrograms Children 6-12 300 micrograms Children < 6 150 micrograms
What is an Acute Kidney Injury?
A rapid decrease in renal function
leads to a fluid/electrolyte imbalance and acid/base disturbance.
RF= age, co-morbidities and medication
What are some of the pre-renal causes of AKI?
Sepsis Hypotension Hypovalemia Renal artery stenosis cardiac liver ACEi
What are some of the intrinsic causes of AKI?
Vasculitis
Glomerulonephritis
Tubular Necrosis
What are the post-renal causes of AKI?
renal tract obstruction (has to be bilateral damage or chronic kidney damage)
What is Nephrotic Syndrome?
Oedema, Protein Urea, hypoalbuminaemia and hyperlipidemia
Over 3.5g of protein
What are some of the causes of nephrotic syndrome?
Deposition Disease Minimal Change Disease Focal and Segmental Glomerulosclerois Membranous Nephropathy Membranoproliferative GN Myeloma ( screen in CKD if >50yrs)
What is Nephritic Syndrome?
Haematuria and Hypertension (+ sub-nephrotic proteinuria)
What is Rapidly Progressing Glomerulonephritis? (RPGN)
Rapid Loss of renal function (usually drops within 50% of eGFR in 3/12)
Formation of glomerular cresents (scars)
can present as Nephritic syndrome.
What is Type 1 RPGN?
Anti-GMB glomerulonephritis
Causes of Type 1 RPGN?
Good Pasteure’s Disease
Anti-GBM disease (same as good pasteures but involves only kidney)
What is Goodpasture’s syndrome?
Anti-glomerular basement membrane disease + pulmonary haemorrhage.
Caused by an anti-body to the alpha-3 chain of type IV collagen
15% of goodpasture’s syndrome is AGBM disease and the rest is ANCA vasculitis
What are common diagnostic features of goodpasture’s syndrome?
Reduced UO haemoptysis oedema SOB cough crackles in lungs nephritic syndrome
What is Type 2 RPGN?
Deposition of immune complexes
What are the causes of RPGN type 2?
SLE, acute proliferative glomerulonephritis and IgA nephropathy, Henoch-Schonlein pupura.
What is type 3 RPGN?
Vasculitis.
Glomeruli are damaged in an undefined manner perhaps through the activation of neutrophils in response to ANCA.
Isolated to glomerulus= primary
Systemic= secondary = ANCA associated vasculitis, granulomatosis with polyangitis, microscopic polyangitis.
What is IgA Vasculitis?
Systemic Also known as HSP Triad of abdo pain, Purpura and arthritis most common vasculitis of childhood get purpuric rash on legs and buttocks can cause intersusseption can cause nephritic syndrome can get IgA nephropathy
What is IgA nephropathy?
Non-aggressive IgA= traditionally slow progression to CKD
Often get episodic haematuria following a sore throat (strep A)
can develop into RPGN
Aggresive IgA= nephritic syndrome 1-4 days post strep A infection
What is Post- Infectious GN?
Get nephritic syndrome several weeks post Strep A infection.
Causes of raised lactate?
Marker of anaerobic respiration or the bodies inability to convert lactate
Sepsis
Ischaemic bowel
Nebulisers ( cause peripheral vasoconstriction)
What are causes of cardiogenic shock in a neonate?
Duct dependent heart disease- baby okay until the duct closes.
left-sided obstructive lesion= shocked (eg aorta coarctation)
right sided obstructive lesion= blue
transposition of the great arteries= blue +/- acidosis
What raises your suspicion of metabolic disease in a neonate?
Hypoglycaemia
hyperammonia
marked lactate acidosis
FHx
How to you calculate plasma osmolality?
2x (Na+ and K+) + urea + glucose
What are the symptoms and signs of pyloric stenosis?
Vomiting after every feed + hungry after vomiting
palpable olive shaped mass, whilst feeding
dehydration
metaolic alkalosis w/hypochloreamia
as kidneys try and correct acidosis by holding onto H+
What is thrombocytopaenia?
A platelet count of less than 150,000/microlitre
What are the causes of Marrow Based thrombocytopaenia ?
1) Malignancy- leukaemia, lymphoma, myeloma or metastatic
2) Viral- infectious mononucleosis, HIV cytomegolovirus
3) Drugs/ Toxins- chemo or heavy alcohol consumption
4) Miliary TB- caseating granulomas within the bone marrow
5) Fibrosis- autoimmune/ inflammatory conditions
What are the sequestrian (enlarged spleen) aetiologies of thrombocytopaenia?
1) Cirrhosis- splenic enlargement may result from LD w/ portal HTN
2) Lysosomal Storage Disease- through splenic enlargement and reduced production
3) Malaria
4) Haematological malignancies
What are the different aetiologies for thrombocytopaenia associated with increased platelet clearance?
1) Immune complex- common differential of exclusion.
2) Medication- Heparin, Abx and anti-epileptics
3) DIC
4) Thrombotic Thrombocytopaenic Purpura - HUS in children and ADAMTSI3 deficiency in adults
5) HEELP- Haemolysis, elevated enzymes and low platelet syndrome= pregnant woman 3rd trimester, pre- /eclampsia.
6) Rheumatological disorders- peripheral estruction of platelets via secondary immune complexes
7) antiphospholipid syndrome- pts w/ lupus anticoagulant may have thrombocytopaenia + a paradoxical prothrombotic state.
8) cyclical thrombocytopaenia- episodeic bleeding every 21-35 days may be associated w/ menstruation.
What is psuedothrombocytopaenia?
1-2% of the population have ethylene diamene tetra acetic acd (EDTA) dependent antibodies.
Causes platelets to clump upon drawing into a EDTA coated blood tube.
Machine doesn’t count clumps as platelets
will have no Hx of bleeding
finger stick peripheral smear will be normal
What are the aetiologies of dilutional thrombocytopaenia?
1) following a blood transfusion- platelets reduce by half following 2 units of RBC. Every 6 units of RBC 1 unit of exogenous platelets should be given.
2) Gestational
What are the aetiologies of Endocrine thrombocytopaenia?
Some inflammatory endocrine conditions can cause iteg Hashimotos
What are the aetiologies of Nutritional thrombocytopaenia?
B12 or folate deficiency cause megoblastic megakaryocyte which can cause it
What is necrotising fascitis?
Bacterial Infection of soft tissue and fascia
Toxins cause thrombosis resulting in quick destruction of tissues
disproportionally painful
high mortality 25% if treated
Clostridium= gas gangrene
often polymicrobial
What is PVL?
Panton- Valentine Leukocidin- a toxin produced by some staph aureus that produce recurrent boils and abscesses- often dermonecrotic.
Can cause pneumonia- it is toxic to WCC therefore be aware of ‘viral chest infection’ with reduced WCC, neg CXR and high CRP.
Explain about Subarachnoid Haemorrhage.
Symptoms
Investigations
maximum intensity w/ 10 seconds- may last a few days at least a few hours
2/3 associated neurological symptoms or clinical findings
may have kernig/ bridzinki’s sign
3rd nerve palsy- posterior communicationg artery aneurysm
Bilateral leg weakness w/ ant communicating artery.
Neurological features are caused by secondary vasospasm which lead to tissue ischaemia.
Inv/ FBC, clotting and U&Es, glucose
ECG can look like an STEMI due to circulating catecholamines.
CT (white= acute blood)
LP = xanthochromia
Explain about central venous thrombosis?
Symptoms
Management
Presents as raised ICP w/headache and papilloedema
mimick a stroke/TIA
seizures
common in younger females (20-35)= pill and pregnancy
management heparin then (6/12 warfarin)
Explain about Viral Encephalitis
Symptoms
Treatment
Headache, fever, meningisum, focal neurology, altered mental state, seizures
Herpes Simplex- acyclovir 10mg/kg
Explain about brain abscess
Symptoms
cause
typical triad= fever, headache and lethargy
specific neurology depends on site
source is usually direct infection or via blood
usually staph or strep
What is central pontine myelinolysis?
occurs inconsistently as a complication of severe ad prolonged hyponatremia particularly if corrected too rapidly
characterised by acute paralysis, dysphagia and dysarthria
What is septic shock?
Sepsis w/
1) persistent hypotension requiring vasopressors to maintain MAP >65
2) serum lactate >2 despite adequate fluid resuscitation
What are the signs of a shaken baby?
Retinol Haemorrage
Encephalopathy
Subdural haematoma
Apnoea
Explain an extra dural haematoma?
Cause
Symptoms
Investigations
Management
low impact trauma LOC period of lucidity rapid decline of consciousness Fixed dilated pupil (3rd nerve compression) Looks bright and like a lens on CT Craniotomy and Evacuation
Explain an acute sub-dural haematoma?
Cause
Symptoms
Investigations
Management
Trauma (high speed or acceleration/deceleration) but can be vascular
wide range of presentation - asymptomatic to comatosed
CT bright and crescent shaped.
Decompression craniectomy
Explain an chronic subdural haematoma?
Cause
Symptoms
Investigations
Management
Elderly, alcoholics, anti-coagulated and infants.
Typically presents several weeks after a mild head injury with progressive confusion, LOC, weakness or higher cortical function.
CT= dark crescent shape
Tx= burr hole drainage
Explain an intracerebral haemorrhage ?
Cause
Symptoms
Investigations
Management
HTN, vascular lesion, cerebral amyloid amgiopathy, brain tumour or infarct.
Presents similar to an ischaemc strole or with decrease in consciousness.
CT bright within the brain matter
Conservative care- may need to evacuate clots.
explain an intraventricular haemorrhage? Cause Investigations Complications Management
Children= prematurity (Neonates in first 72hrs of life unknown aetiology)
Adults= linked to subarachnoid, vascular lesions or tumours.
CT bright within th edark CSF spaces of the ventricles.
Risk of obstructive hydrocephalous- surgical intervention
What is placenta percrete?
when the placenta erodes through the myometrium of the uterus.
The most severe case is when it evades into the bladder.
Explain Meckel Diverticulum.
2%- occurs in the population 2inches- long 2- feet from the ileocaecal valve 2/3 have ectopic mucosa 2 types of ectoptic tissue are commony present (mostly gastric and pancreatic) 2% become symptomatic.
Why does Prothrobin time increase in biliary obstruction?
Have a decrease in concentration of bile salts, this leads to poor vit K absorption.
Explain about Bilirubin
It is a breakdown product of Hb
An isolated rise is likely to be due to an inherited bilirubin metabolism defert, haemolysis or ineffective erythropoiesis.
Hyperbilirubinaemia causes by hepatobillary disease is almost always accompanied by another abnormality.
Explain about aminotransferase
Enzymes present in hepatocytes and they leak into the blood w/liver cell damage.
Asparte Aminotransferase is also present in heart and skeletal muscle
Alanine Aminotransferase is more specific to the liver
Explain about Alkaline Phosphate
Situated in the canalicular and sinusoidal membranes of the liver.
Raised serum concentrates are seen in cholestatis regarless of whether its an intra or extra hepatic causes .
Also found in placenta or bone.
Explain about Gamma GT
A liver microsomal enzyme which may be induced by alcohol and enzyme inducing drugsc
In cholestasis the Gamma GT rises in parallel w/ ALP as they excreted similarly.
How do you interpret abnormal liver biochemistry?
1) Predominant rise in serum aminotransferase indicates hepatocellular injury
2) elevation in serum bilirubin and ALP in excess of aminotransferase= cholestatic disease
What are the prehepatic causes of jaundice?
Haemolysis (unconjugated)
What are intrahepatic but unconjugated cause of jaundice?
Gilberts Disease
only abnormality is an isolated rasied Bilirubin.
What is cholestatic jaundice?
Presents with jaudice w/ conjugated bilirubin, pale stools and dark urine.
Split into:
Intrahepatic= caused by hepatocellular swelling in parenchymal liver or abnormalities at cellular level of bile excretion
Extrahepatic= obstruction of bile flow at any point distal to the bile canaliculi
What are some of the intrahepatic causes of cholestatic jaundice?
Viral Hepatitis Drugs Alcoholic Hepatitis Cirrhosis Pregnancy Recurrent Idiopathic Cholestasis Infiltrations Congenital
What are some of the extrahepatic causes of cholestatic jaundice?
Common duct stones Carcinoma (bile duct, pancrease,ampulla) Biliary stricture sclerosing cholangitis Pancreatitis Pseudocyst
Explain Hepatitis B serology
HBsAg
anti-Hbc
anti-HBs
IgM-HBc
HBsAg anti-HBc anti-HBs IgM anti-HBc
Immune (Nat) -ve . +ve . +ve . -ve
Immune (vac) . -ve . -ve . +ve . -ve .
Acute Inf . +ve . +ve . -ve . +ve
Chronic Inf . +ve . +ve . -ve . -ve
HBeAg = infective
What is the criteria for a TIA?
Stroke but symptoms resolve in 25hrs
Explain a total anterior circulation infarct
- which arteries are involved
- what symptoms would you expect?
involved the middle and cerebral arteries
all 3 oxford stroke classifications would be present .
explain Partial Anterior circulation Infarcts
- which arteries are involved
what symptoms you’d expect?
Involves smaller arteries of the ant. circulation.
2 of the oxford stroke classification would be present.
explain lacunar infarcts
- which arteries are involved
what symptoms would you expect?
involves perfortating arteries around the internal capsuale, thalamus and basal ganglia.
Presents with 1 of the following.
unilateral weakness (+/- sensory) of face and arm, arm and leg or all three.
Pure sensory stroke
ataxic hemiparesis
What factors does warfarin inhibit?
Vit K dependent factors
II, VII, IX, X
What is Addison’s disease?
Autoimmune destruction of the adrenals
80% causes of hypoadrenaline
What are the symptoms of Addisons disease?
lethargy, weakness, anorexia, N&V, weightloss, “salt-craving”, hyperpigmentation (palmar crease first), femal loss of pubic hair, hypotension.
Hyponatramia
Hyperkalaemia
Hypercalcaemia
What is primary hypoparathyroidism?
Reduced PTH secretion
eg. due to thyroid surgery
What is the ion profile of primary hypoparathyroidism?
Low Calcium
High Phosphate
What are the symptoms of primary hypoparathyroidism?
secondary to hypocalcaemia, tetany, perioral paraethesia, trousseau’s sign, chrostek’s sign. ECG prolonged QT interval.
What are the signs of Wernicke’s Encephalopathy?
CAN OPEN Confusion Ataxia Nystagmus Ophlamoplegia PEripheral Neuropathy.
Expressive Language Milestones? 6 months 9months 12 months 20months 24 months 36 months
6 months- vowel sounds 9 months- babbling (mamma/dada) 12 months- first word with meaning 20 months- 20/30 words 24 months >50 words, joins 2-3 36 months- short sentences
Receptive Language Milestones? 5 months 7 months 11 months 14 months 18 months 24 months
5 months- responds to name 6-7 months- momentarily stops to 'no' 11 months- stops action when told no 14 months- 1 step command 18 months- points to objects when named 24 months- 2 step command
Fine motor milestones? 3 months 6 months 8 months 12 months 18 months 24 months 36 months
3- open and clasps hands 6- holds bottle with 2 hands 8 months- holds finger food 1 hand 12 months- transfers objects 18- scribbling etc (3 block tower) 24 months holding crayon (6-7 block tower) 36 month copy circle (9 block tower)
Gross motor milestones? 3 months 4 months 6 months 9 months 11 months 12 months 18 months 24 months 30 months 36 months
3- hold head up straight 4- roll over front to back 6- sit without support 9- crawling 11- cruising 12- walking (first step) 18- walking well 24- runs, climbs stairs 30-jump 36- climbs stairs with alternate feet.
How do you stage lymphoma?
A= no B symptoms B= b symptoms
1= 1 lymph node only
II= >2 LN same side of the diaphragm,
III= LN and/or spleen AND on both sides of the diaphragm
1. above renal vessels
2. in lower abdomen
IV= extranodal involvement (e/g liver and lungs)
What are the indications for dialysis in an AKI?
uraemia= obtundation, astrixis, seizures, nausea, vomiting or pericarditis
hyperkalaemia that cannot be medically managed (>6.5 mmol/L if ECG changes)
fluid overload reisitant to diuretics
metabolic acidosis that cannot be medically managed.
pH <7.2 despite Sodium Bicarbonate therapy (cannot have if fluid overloaded)/
What are some pre-hepatic causes for portal hypertension?
congenital atresia/stenosis
portal/splenic verin thrombosis
extrinsic compression eg pancreatic tumour
What are some hepatic causes of portal hypertension?
Cirrhosis
Chronic Hepatitis
Myeloproliferative disease
What are some post hepatic causes of portal hypertension?
Budd- Chiari Syndrome
Constructive Pericarditis
RHF
Haemophilia A is which factor deficiency?
VIII
Haemophilia B is which factor deficiency?
IX
Haemophili C is which factor deficiency?
XI
MYOTOMES;
C5
elbow flexion
MYOTOMES
C6
wrist extension
MYOTOMES
C7
elbow extensors
triceps
MYOTOMES
C8
finger flexors
MYOTOMES
T1
small finger adductions
MYOTOMES
L2
hip flexors
MYOTOMES
L3
knee extensors
MYOTOMES
L4
ankle dorsiflexors
MYOTOMES
L5
big toe extensors
MYOTOMES
S1
ankle plantar flexors
How do you medically treat hyperkalaemia?
1) is the pt passing urine- no= dialysis
2) 5.5-6.5- no risk of CA 6.5-7.5 treat if ECG changes. 7.5= medical emergency.
3) IV Ca gluconate 10ml of 10%. Beta agonist 10mg salbutamol via neb, 10 units of insulin + glucose
Sodium bicarb to correct acidosis.
What is the oxford stroke classification?
1) unilateral hemiparesis and/or hemisensory loss of the face, arm and leg
2) homonymous hemianopia
3) higher cognitive dysfunction (eg dysphagia)
Explain Posterior Cerebral Infarcts
which vessels are involved
what symptoms would you get?
1) cerebellar brainstem syndromes
2) loss of consciousness
3) isolated homonymous hemianopia
Features of class 1 haemorrhagic bloodloss?
<750ml <15% bloodloss <100 HR BP normal pulse pressure normal RR= 14-20 min UO >30ml/hr CNS= slighlt anxious
What does RA look like on an x-ray?
loss of joint space
erosions
soft tissue swelling
soft bone tissue (osteopenia)
what does OA look like on an x-ray?
loss of joint space,
osteophytes
subcondral sclerosis
subchondral cysts
What spinal tracts are affected in syringomelia?
what are the clinical features?
Ventral Horns, lateral spinothalamic tract
flaccid paresis typically effecting the intrinsic hand muscles
loss of pain and temperature sensation.
what spinal tracts are affected in MS?
what are the clinical features?
Asymmetrical, varying spinal tracts
combination of motor, sensory and ataxia symptoms.
What are the spinal tracts affected and the clinical features of Anterior Spinal artery occlusions.
lateral corticospinal tracts
lateral spinothalamic tracts
Bilateral spastic paresis
bilateral loss of pain and temperature.
What are the spinal tracts affected and the clinical features in subacute combined degeneration of the spinal cord?
so a B12 and folate deficiency
1) lat. corticospinal tracts, dorsal column and the spinocerebellar tract
bilateral spastic paresis
bilateral loss of proprioception and vibration sensations
bilateral limb ataxia.
What are the spinal tracts affected and the clinical features of Brown-Sequard syndrome?
Spinal cord hemisection
1) lateral corticospinal, dorsal coluns and the ;lateral spinothalamic tract.
ipsilateral spastic paresis below the lesion
ipsilateral loss of proprioception and vibration sensation
contralateral loss of pain and temperature.
What are the features of class IV haemorrhagic shock?
>2000ml bloodloss >40% circulating volume >140 HR low BP low pulse pressure RR= 35/min urine output negligible CNS confused/ lethargic
What are the features of class III haemorrhagic shock?
1500-2000ml bloodloss 30-40% bloodloss 120-140 HR BP decreased pulse pressure decreased RR= 30-40 urine output 5-15 mls CNS= anxious, confused
What are the features of class II haemorrhagic shock?
750-1500ml (15-30%) lost HR= 100-120 BP normal pulse pressure= decreased RR= 20-30/min UO 20-10 ml/hr CNS anxious
What is the hormone profile for primary hyperparathyroidism?
Raised = PTH and Ca 2+ Decreased= PO3-
What are the clinical features of primary hyperparathyroidism?
mild: asymptomatic
recurrent abdo pain (pancreatitis, renal colic)
what are the causes of primary hyperparathyroidism?
solitary adenoma
multifocal adenoma
carcinoma
what are the treatment options for primary hyperparathyroidism?
surgery if indicated e.g age. life-threatening, osteoporosis.
What is the hormone profile for secondary hyperparathyroidism?
Raised= PTH, PO3-
Ca2+ normal or decreased
Vit D decreased
What are the symptoms of secondary hyperparathyroididm?
few symtoms may have- bone disease, osteitis, fibrosa cystica and soft tissue calcification
What is the cause of secondary hyperparathyroidism?
hyperplasia as a result of low calcium, almost always as a result of chronic renal disease.
What is the hormone profile for tertiary hyperparathyroidism?
Raised PTH, ALP and maybe Ca2+
Po3-/ Vit D are normal or decreased
what are the clinical features of tertiary hyperparathyroidism?
metastatic calcification, bone pain/fracture, nephrolithiasis, pancreatitis
what are the causes of tertiary hyperparathyroidism?
ongoing hyperplasia of PT gland after correction of the underlying renal disease.
How does Warfain effect
1) Prothrobin Time
2) APTT
3) Bleeding time
4) Platelets
1) increases
no effect on the others
How does Aspirin effect
1) Prothrobin Time
2) APTT
3) Bleeding time
4) Platelets
3) increases
no effect on the others
How does Heparin effect?
1) Prothrobin Time
2) APTT
3) Bleeding time
4) Platelets
1) may increase
2) increases
no effect on the others
How does DIC effect?
1) Prothrobin Time
2) APTT
3) Bleeding time
4) Platelets
1) increases
2) increases
3) increases
4) decreases
What are the myeloma defining events?
C- hyperCalcaemia
R- Renal Insufficiency
A- Anaemia
B- Bone lesions
None of which can be explained by another cause
What is myeloma?
Plasma cell neoplasm
How would a sub-dural lead to a nerve palsy?
mass shift and herniation which occludes 3rd cranial nerve
1st= parasympathetic= blown pupil
2nd= occlusion of whole nerve= down and out pupil.
Pupil Sparing 3rd nerve palsy= normally a medical cause/
Causes of Carotid Artery Disection?
Spontaneous- elderly
Trauma- high speed, delayed onset of Sx.
Causes ischamia to brain and stroke- like symptoms
Cause and effect of diffuse axonal damage?
Normally unconcious from impact
high impact acc/deceleration trauma, especially including rotation
long term survivors= loss of white matter+ enlarged ventricles, alzheimer like pathology.
What are the functions of the kidney?
Filtration/ excretion Acid- Base buffering (kidney produces HCO3-) EPO secretion Electrolyte Balance activates Vit D RASS- fluid and BP
What are the effects of CKD?
Reduced GFR= Raised K+ and Creat
Acidosis (reduced acid removal)
reduced EPO secretion= anaemia
renal bone disease- reduced Ca, Increased Phosphate, increased parathyroid (2ndary hyperparathyroidism)
impaired BP regulation- HTN
reduced fluid removal- oedema
impaired iron absorption- iron deficiency
reduced clearance of gastrin- peptic ulceration
What are the indications for dialysis?
Refractory Pulmonary Oedema Refractory Hyperkalaemia Refractory Acidosis Uraemic Encephalitis Pericarditis
What is ANCA?
Anti-Neutrophil Cytoplasm Antibodies
C-ANCA: PR3 (proteinase 3) cytoplasm staining
P-ANCA: MPO (myeloperoxidase) around the nucleus
What are the ANCA associated vasculitis?
1) granulomatosis w/polyangitis
2) microscopic polyangitis
3) eosinophillic granulomatosis w/polyangitis (Hx of atopic lung disease)
What are the large vessel vasculitis?
Giant Cell Arteritis
Takayasu (woman of childbearing age- granulmatosis of aorta + major branches. Get systemic inflammation then a pulseless phase of vascular insufficiency)
What are the medium vessel vasculitis?
Kawasaki (under 5, fever >5 days, lymphadenopthy, rash genitals, red mucus membranes, Polyarteritis Nodosa (systemic, necrostising vasculitis, microaneurysms for a rosary sign)
What are the small vessel vasculitis?
ANCA associated
Immune Complex Cryoglobulinaemic IgA ( HSP) HUV Anti-GBM
What is Anti-phosphide lipid syndrome?
Autoimmune, hypercoaguble state causes by anti-phospholipid anti-bodies.
Provokes both arterial and venous thrombosis
Causes severe pregnancy related complications including miscarriage, still birth and eclampsia.
Can be Primary or secondary (With SLE)
Treat with an anti-coagulant (NB not warfarin in pregnancy as it can cross placental barrier and is tetragenic)
What are some of the pre-renal causes of CKD?
RAS (discrepency of >1cm in kidney size think) , nephrosclerosis + ACEi
What are some of the intrinsic causes of CKD?
GN, TIN (tubulointerstital Nephritis), ADPKD
What are some of the post-renal causes of CKD?
BPH, RPF (renal blood flow)
How to pre-renal, renal and post renal causes of kidney disease differ on urine dip?
Renal has urine dip +ve for blood and protein.
Pre and post are clear
NB- urine may be contaminated by blood from cancer ot stone in Post,
What are the indications to investigate HTN further?
Onset before 30 Proteinuria, haematuria, glycosuria Abnormal Biochemisty Severe, resistant HTN clinical features of an underlying cause
What are the causes of secondary HTN?
RENAL:
Polycystic KD: cysts prevent normal functioning
Glomerular Disease
Diabetic Neuropathy: Damages the small capillaries
VASCULAR:
Reno-vascular HTN: RAS either atherosclerosis or fibromuscular dysplasia
Coarctation of the aorta
ENDOCRINE:
Cushings: Adrenal Gland increase cortisol
Aldosteronism (Conn’s)= kidneys retain Na+ and H2O, secrete K+ therefore raised BP
Pheochromocytoma= increased production of adrenaline and noradrenaline
Thryroid= both hyper and hypo
Hyperparathyroidism: increased Ca2+
OTHERS:
Drugs
Pregnancy
Sleep Apnoea= hypoxia leads to damage to vessels walls there for less effective at regulating BP.
What is Addison’s disease?
How would you test for it?
hypocortisol and adrenal insufficiency
Measure 8am cortisol- Low = adrenal insufficiency
Cosyntropin stimulation test: measure base ACHT test.. administer synacthen (synthetic ACHT) low cortisol+ high ACTH= primary (adrenals) low cortisol + low ACTH= secondary (pituitary)
What is the difference between Cushing’s disease and Cushing’s Syndrome?
Cushings Disease is raised ACTH from a pituitary cause
Cushings Syndrome is just raised cortisol
How do you diagnose Cushing’s?
1) ACHT level
- low= ACHT independent
- high= ACHT dependent
2) ACHT independent= CT scan/MRI abdomen
- Adrenal adenoma/adrenal cancer
- bilateral hyperplasia
3) ACHT dependent = inferior petrosal sinus and MRI brain + CXR
- pituitary tumour (cushing’s disease)
- ectopic ACHT tumour (lung/thymus).
What is hyperglycaemic, hypersosmolar syndrome?
type 2 diabetic (unwell not take medication)
increase in glucose= increase in diueresis = dehydration
No frank ketoacidosis (enough insulin)
What are the causes of lymphadenopathy?
REACTIVE:
Infective: Bacterial (tonsillitis, cellulitis, TB, primary syphillis), Viral (EBV, CMV, HIV, hepatitis), Other (toxoplasmosis)
Non-infective: Sarcoidosis, amyloidosis, connective tissue disease (RA, SLE), dermatological (eczema, psorasis), drugs (phenytoin, retroviral drugs)
INFILTRATIVE:
Benign Histiocytosis
Neoplastic: Haemotological ( Hodgekins, Non-hodgekins lymphoma, CML,CLL, ALL,AML)
Causes of Hepatomegaly?
SMOOTH AND TENDER: alcoholic hepatitis, Tricuspid regurgitaion w/RHF. Infectious Hepatitis ( acute infection) , RHF/PE, Glandular Fever, Budd-Chiari Syndrome, Abcess.
SMOOTH BUT NOT TENDER: Amyloidosis, leukaemia, early cirrhosis, lymphome, haemochromatosis, Primary Biliary Cholangitis, Fatty Liver, HIV, Sarcoidosis
IRREGULAR AND NON-TENDER: Neoplastic ( Hepatoma, metastatic carcinoma), hyatid cyst, polycystic liver
Causes of Splenomegaly?
FEVERS: Infection (malarie, IE, hepatitis, EBV,TB, CMV, HIV), sarcoid, malignancy (lymphoma, chronic leukaemia)
LYMPHADENOPATHY: Glandular Fever, leukaemias, lymphomas, Sjogren’s Syndrome
PURPURA: Amyloid, Septicaemia, Typus, DIC, Meningiococcaemia
ARTHRITIS: Sjogren’s, RA, SLE, Lyme’s Disease, Vasculitis
ASCITES: Carcinoma, Portal Hypertension
MURMUR: IE, Rhuematic Fever, Hypereosinophillic syndrome, amyloid
MASSIVE SPLENOMEGALY: Malaria, CML, myelofibrosis, leishmaniasis, Gaucher’s
WEIGHT LOSS AND CNS PATHOLOGY:
Cancer, lymphoma, TB, myeloma, arsnic poisoning
ANAEMIA: Haemolytic Anaemia, leishmaniasis, leukaemia, pernicious anaemia.
Causes of Hypercalcaemia?
ENDOCRINE:
Excess PTH: Primary and Tertiary Hyperparathyroidism, Ectopic Parathyroid Hormone
Other: Thyrotoxicosis and Addison’s Disease
MALIGNANT: Myeloma, Bone Mets
EXCESS ACTION OF VIT D: lymphoma, granulomatous disease (sarcoid/TB), self administered Vit D
DRUGS: Thiazides, Vut D analogues, Lithium and Vit A
OTHER: long term immobility, familial hypocalciuric hypercalcaemia.
