General Flashcards
Difference between ARPKD and ADPKD
-AR PKD is more severe, comes on at a younger age. Is autosomal recessive
-AD PKD usually comes on in adulthood and is less severe. Autosomal dominant
How might a patient with PKD present
Incidental
Raised BP
Picked up on examination
Family screening
Abdo pain
Haematuria
Recurrent UTIs
May present with a haemorrhagic stroke
Extra renal manifestations of PKD
Liver/pancreas/ spleen/ovarian cysts
Cardiac valve disease
Aortic dilatation/ aneurysm
Cerebral aneurysms
Abdominal wall hernias
What is the most commonly affected valve in IE
Tricuspid
Commonly associated bacteria in IE
-Staph Aureus
-Streptococcus (usually of the viridians group)
-Enterococci
Other causes of enlarged kidneys
-PKD
-Hydronephrosis
-Infiltration (eg amyloid)
-Tumours
-Congenital
Management of PKD
1st- renoprotective lifestyle measures
-eg healthy diet/ BP optimisation/ excercise/ stop smoking / low salt
2st Tolvaptan (if rapidly progressing disease)
3rd Manage HTN / UTIs
4th Surgical intervention
-nephrectomy
-embolisation of bleeding cysts etc
5th RRT / Renal transplant
SPK indication
T1DM with nephropathy
Some T2DM if they meet certain criteria
SPK - are pancreas and kidney always done at same time?
No
Sometimes done simultaneously, other times may be done successively
Complications of SPK/ transplants
Acute
-Hyperacute rejection- needs nephrectomy
-Bleeding
-Infection
-Pain
Subacute
-Graft pancreatitis
-Peri-pancreatic collections
-Acute rejection (Mx steroids)
-PTLD
-Reactivation of infections eg BK virus
-Side effects from immunosuppression
Chronic
-gradual decrease in graft function (HTN/ proteinuria)
-recurrence of original disease
Where is the pancreas drained into in an SPK?
Drained into the duodenum /enteric drainage to avoid complications
How can you assess for encephalopathy?
-Check for the presence of asterixis
-Check constructional apraxia, e.g. ask the patient to draw a 5 pointed star
Scoring systems in cirrhosis?
Child Pugh
Meld (for transplant planning)
grading of encephalopathy
uses the west haven criteria
-Grade 0-4
0-some changes to memory
1- mild confusion
2-drowsiness/ lethargy
3-solomnent but rousable
4-comatose
complications of CLD
-varices, haemorrhage
-clotting disorder and abnormal bleeding/bruising
-hypoalbuminaemia leading to ascites/ peripheral oedema
-portal hypertension
-SBP
-Hepatorenal syndrome
management of ascites
- fluid restrict and diuretics
- ascitic drain with HAS
- refractory ascites-> TIPSS and liver transplant
Complications of TIPSS
-coagulopathy
-encephalopathy
causes of gynaecomastia
lack of androgens
-CLD
-Testicular atrophy or failure
-Klinefelters
-Drugs e.g. Mineralocorticoid agonists/ digoxin
-physiologically in puberty/ later life
Causes of decompensation in CLD
-ALcohol binge
-Sepsis / infection of other cause
-SBP
-Dehydration
-Constipation
-GI bleeding
-Reactivation of infection (eg Hep B) or new infection
-Drugs (eg paracetamol/ methotrexate)
-Clots (PVTs)
-HCC
management of decomposition CLD
-ABCDE
-Refer to the BASL guideline
-Identify and treat cause of decompensation
-Bloods , incl NILS, clotting, albumin, bilirubin
-Tap ascites (PMN/ albumin/ MCS)
-ETOH HX, put on CIWA and lorazepam if necessary and manage withdrawal
-monitor fluid balance
-Optimise nutrition / NG feeding / dietician
-Ensure opening bowels (lactulose / enemas)
-Manage electrolyte abnormalities
-Identify GI bleeding-> will need scope + mx this
-correct clotting
-LMWH prophylaxis
-get specialist input
-early referral to ICU if not improving
signs of chronic pancreatitis on exam?
fentanyl patches
abdo tenderness - particularly at epigastrium
complications of pancreatitis
-chronic pancreatitis and chronic pain
-pancreatic pseudocysts which may compress/ obstruct near by structures
-peri-pancreatic collections
-strictures
-thromboses
-pancreatic malignancy (chronic)
-SIRS (acute)
causes of pancreatitis
IGETSMASHED
I-idiopathic
G-gallstones
E-ethanol
T-trauma
S-steroids
M-mumps
A-autoimmune conditions/ genetics
S-scorpion stings
H-hypertriglyceridaemia/ hypercalcaemia
E-ERCP
D-drugs including azathioprine.
management of pancreatitis
Acute- pain, fluids
Supportive
Chronic
-pain management
-manage complications (eg check DM / pancreatic insufficiency/ manage strictures/ blockages etc)
-dietitian input (creon/ vitamins inc/ electrolytes - esp Magnesium. Vit D)
if you see a stoma on exam - to complete your examination you should say..
I’d like to examine the stoma in closer detail with the bag removed. And potentially perform a rectal examination of the stoma
What is glomerulonephritis
Inflammation in the glomeruli
-can cause a nephritic or nephrotic picture
Causes of glomerulonephritis
-Bergers disease (IgA nephropathy)- most common cause
-Membranous nephropathy- causes nephrotic syndrome (e.g idiopathic/ 2ry to malignancy/ SLE)
-Membranoproliferative glomerulonephritis
-post streptococcus glomerulonephritis
-cresenteric / rapidly progressive glomerulonephritis (can be caused by SLE/ p/canca)
Nephritis can be caused by systemic disease e.g.
-HSP
-p-anca and c-anca related vasculitis \
treatment of glomerulonephritis
treat underlying cause
supportive
immunosuppression
manage complications
RRT
Management of Addisons
Acute crisis-> High dose steroids
Intercurrent illness->double dose steroids
Long term -> glucocorticoid plus mineralocorticoid
Investigation of Addisons
->9am cortisol
->short synACTHen test
->Urea and electrolytes
-> BM and BP
Postural orthostatic tachycardia syndrome
Causes syncope- disorder of autonomic system
Causes tachycardia on standing
How is HHT inherited?
Autosomal dominant
How may HHT present?
Recurrent nose-bleeds
Anaemia
GI bleeding
Haemoptysis
How is Friedreich’s ataxia inherited?
Autosomal recessive
HHT complications
AV malformations
-Brain
-Gut
-Liver
-Lungs
Nosebleeds
HHT investigations
Bedside- Obs
Bloods- Hb/ plt/ clotting /haematinics/ blood film
Special -
Gut- OGD/colonoscopy
Brain- CTA/ MRA
Chest- CT chest/ CXR / ABG
Liver- USS / LFTs
Genetic tests
HHT management
Nosebleeds-
topical treatments
advise on humidification
ointments
refer to ENT
Gut
-Endoscopy-> ablation ?
Liver
-Screening. optimisation. if recurrent disease then ? liver transplant
Optimise iron stores
-iron replacement/ dietician
avoid tea after meals etc
What is achalasia?
Failure of relaxation of the lower oesophageal sphincter
achalasia management
-conservsative
(eg nitrates)
-surgical
(eg balloon dilatation/ cardiomyotomy)
-botox injections
PEG feeding
management of C1 esterase inhibitor
- give the enzyme inhibitor as a concentrate
- avoid triggers + pt education
- treat underlying disease (e.g. malignancy/ SLE)
-treat as anaphylaxis
LESS in RA
L- oss of joint space
E-periarticular erosions
S-soft tissue swelling
S-soft bones (osteopenia)
LOSS in OA
L-oss of joint space
O-osteophytes
S-subchrondral cysts
S-subchondral sclerosis
management of AIP
haemin
supportive care
patient education
genetic screening
Features of Friedreichs ataxia
-Ataxia
-Loss of vibration and proprioception
-Hypertrophic Cardiomyopathy (may have ICD)
-Diabetes
Signs of a common peroneal nerve palsy
Observe:
Foot drop/ high stoppage gait
Check fibula head / knee for scars
Power:
Weak dorsiflexion/ eversion
Sensation:
Check anterolateral leg and dorm of foot and 1st web space
Origin of common peroneal nerve
L4/L5
Causes of common peroneal nerve lesion
-> compression / trauma
->vasculitis
->any cause of peripheral neuropathy
How to differentiate common perineal nerve palsy from L5
Check sensation at bottom of foot (L5 lesion would be lost)
Cannot SLR in L5 lesion
sensory vs cerebellar ataxia ?
Sensory-
Rombergs
or Pseudoathetosis (fingers moving which gets worse when eyes closed)
Dorsal column involvement (loss proprioception/ vibration)
Cerebellar
-Scanning speech
-Truncal ataxia
-Nystagmus and other ocular signs
CM1 and CM2
CM1 - demyelinating
CM2 - axonal
Define bronchiectasis
obstructive lung condition characterised by dilatation and destruction of the bronchi caused by chronic infection or inflammation
stages of diabetic retinopathy?
Pre-proliferative
Mild- micro aneurysms only
Moderate- micro aneurysms + hard exudates + cotton wool spots
Pre-proliferative / severe , features of moderate + intra-retinal microvascular abrnormalities + venous beading
Proliferative- neovascularisation / vitreous haemorrhage
differentials for diabetic retinopathy
macular degeneration
vitreous haemorrhage
cataracts
hypertensive retinopathy
migraine
TIA
ocular associations with diabetes
retinopathy
macular oedema
cataracts
vitreous haemorrhage
central retinal vein occulsion or central retinal artery occlusion
higher risk of glaucoma
TIA
stroke
investigations in Myasthenia
Anti cholinesterase receptor antibodies
Anti MUSK antibodies
TFTS
emg
CT chest to check for Thymoma
FVC if acute
what could trigger a myasethenic crisis?
infection
dehydration
stress
non compliance with medication
trauma
anaemia
drugs
name some types of muscular dystrophies
-myotonic dystrophy
-limb-girdle muscular dystrophy
-Duchennes muscular dystrophy/beckers
-facioscapulohumeral dystrophy
What is the PESI score
Pulmonary Embolism Severity Index score
Takes into account:
HR, BP, O2 ,Co-morbs including: lung disease/ cancer
Age
Can classify risk in patients who have a diagnosis of PE and highlight which ones may need to be escalated to higher levels of care (e/g ICU)
grading of thyroid eye disease
NO SPECS
N-no signs or symptoms
O- only signs
S-soft tissue involvement
P-proptosis
E-extraoccular muscle involvement
C-corneal involvement
S-sight loss
early signs of Parkinson’s
constipation
trouble sleeping
falls
tremor
management of Parkinson’s
L Dopa w/ peripheral dopamine de-carboxylase inhibitors
Dopamine agonists
COMT inhibitors
Anticholinergics
MAO B inhibitors
MDT
SLT , dieticians, psychiatry, pt, ot
Surgical
Deep brain stimulation
Dopamine pumps
Diagnosis of PD
clinical diagnosis
Structural brain imaging to rule out other causes EG stroke/ NPH / SOL/ parkinsons plus syndromes
triad of Parkinsonism
Resting tremor
Bradykinesia
Rigidity
how to present a PD case
This patient has a hypo mimic phase with hypophonia, there was a resting assymetrical tremor. There was lead pipe rigidity and cog wheeling in the arms
power and sensation and reflexes were normal
there was a stooped posture and reduced arm swing with walking. there was a shuffling gait
there were/ were not signs of a Parkinsons plus syndrome
How to describe the movement of hands in PD
reduction in frequency and amplitude of movements
NYHA scoring
Class 1- not limited
Class 2- limited on activity
Class 3- limited on light activity , only comfy at rest
Class 4- symptoms at rest
a cushingoid appearance…
moon shape facies
abdominal straie
aganthosis nigricans
thinning of the arms and legs
central adiposity
gynaecomastia
buffalo hump
thin skin
bruising
Scoring systems in TIA
ABCD2 score
Estimates risk of stroke after having a TIA
Takes into account
A age
BP
C clinical symptoms of stroke
D duration of symptoms
Function of the spleen
Filtration of the blood
Iron metabolism
Extra medullary haematopoesis
Storage of RBCs and platelets
Causes of central loss of vision
Macular degeneration
Macular disease (eg from DM)
Retinal vein occlusion
Hypertensive retinopathy
Optic neuritis or optic nerve disease
Cataracts
What do you see on fundoscopy for retinitis pigmentosa?
Pigmentary bony spicules
Differentials for a cranial nerve 7 palsy
Bell’s palsy
Ramsay hunt
Sarcoidosis
Cerebellar pontine angle lesion
Acoustic neuroma
Lesion at the cranial nerve nucleus (eg stroke / demyelination)
