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General Flashcards

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1
Q

Difference between ARPKD and ADPKD

A

-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

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2
Q

How might a patient with PKD present

A

Incidental
Raised BP
Picked up on examination
Family screening
Abdo pain
Haematuria
Recurrent UTIs
May present with a haemorrhagic stroke

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3
Q

Extra renal manifestations of PKD

A

Liver/pancreas/ spleen/ovarian cysts
Cardiac valve disease
Aortic dilatation/ aneurysm
Cerebral aneurysms
Abdominal wall hernias

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4
Q

What is the most commonly affected valve in IE

A

Tricuspid

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5
Q

Commonly associated bacteria in IE

A

-Staph Aureus
-Streptococcus (usually of the viridians group)
-Enterococci

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6
Q

Other causes of enlarged kidneys

A

-PKD
-Hydronephrosis
-Infiltration (eg amyloid)
-Tumours
-Congenital

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7
Q

Management of PKD

A

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

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8
Q

SPK indication

A

T1DM with nephropathy
Some T2DM if they meet certain criteria

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9
Q

SPK - are pancreas and kidney always done at same time?

A

No
Sometimes done simultaneously, other times may be done successively

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10
Q

Complications of SPK/ transplants

A

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

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11
Q

Where is the pancreas drained into in an SPK?

A

Drained into the duodenum /enteric drainage to avoid complications

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12
Q

How can you assess for encephalopathy?

A

-Check for the presence of asterixis
-Check constructional apraxia, e.g. ask the patient to draw a 5 pointed star

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13
Q

Scoring systems in cirrhosis?

A

Child Pugh
Meld (for transplant planning)

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14
Q

grading of encephalopathy

A

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

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15
Q

complications of CLD

A

-varices, haemorrhage
-clotting disorder and abnormal bleeding/bruising
-hypoalbuminaemia leading to ascites/ peripheral oedema
-portal hypertension
-SBP
-Hepatorenal syndrome

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16
Q

management of ascites

A
  1. fluid restrict and diuretics
  2. ascitic drain with HAS
  3. refractory ascites-> TIPSS and liver transplant
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17
Q

Complications of TIPSS

A

-coagulopathy
-encephalopathy

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18
Q

causes of gynaecomastia

A

lack of androgens
-CLD
-Testicular atrophy or failure
-Klinefelters
-Drugs e.g. Mineralocorticoid agonists/ digoxin
-physiologically in puberty/ later life

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19
Q

Causes of decompensation in CLD

A

-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

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20
Q

management of decomposition CLD

A

-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

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21
Q

signs of chronic pancreatitis on exam?

A

fentanyl patches
abdo tenderness - particularly at epigastrium

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22
Q

complications of pancreatitis

A

-chronic pancreatitis and chronic pain
-pancreatic pseudocysts which may compress/ obstruct near by structures
-peri-pancreatic collections
-strictures
-thromboses
-pancreatic malignancy (chronic)
-SIRS (acute)

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23
Q

causes of pancreatitis

A

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.

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24
Q

management of pancreatitis

A

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)

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25
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
26
What is glomerulonephritis
Inflammation in the glomeruli -can cause a nephritic or nephrotic picture
27
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 \
28
treatment of glomerulonephritis
treat underlying cause supportive immunosuppression manage complications RRT
29
Management of Addisons
Acute crisis-> High dose steroids Intercurrent illness->double dose steroids Long term -> glucocorticoid plus mineralocorticoid
30
Investigation of Addisons
->9am cortisol ->short synACTHen test ->Urea and electrolytes -> BM and BP
31
Postural orthostatic tachycardia syndrome
Causes syncope- disorder of autonomic system Causes tachycardia on standing
32
How is HHT inherited?
Autosomal dominant
33
How may HHT present?
Recurrent nose-bleeds Anaemia GI bleeding Haemoptysis
34
How is Friedreich's ataxia inherited?
Autosomal recessive
35
HHT complications
AV malformations -Brain -Gut -Liver -Lungs Nosebleeds
36
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
37
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
38
What is achalasia?
Failure of relaxation of the lower oesophageal sphincter
39
achalasia management
-conservsative (eg nitrates) -surgical (eg balloon dilatation/ cardiomyotomy) -botox injections PEG feeding
40
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
41
LESS in RA
L- oss of joint space E-periarticular erosions S-soft tissue swelling S-soft bones (osteopenia)
42
LOSS in OA
L-oss of joint space O-osteophytes S-subchrondral cysts S-subchondral sclerosis
43
management of AIP
haemin supportive care patient education genetic screening
44
Features of Friedreichs ataxia
-Ataxia -Loss of vibration and proprioception -Hypertrophic Cardiomyopathy (may have ICD) -Diabetes
45
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
46
Origin of common peroneal nerve
L4/L5
47
Causes of common peroneal nerve lesion
-> compression / trauma ->vasculitis ->any cause of peripheral neuropathy
48
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
49
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
50
CM1 and CM2
CM1 - demyelinating CM2 - axonal
51
Define bronchiectasis
obstructive lung condition characterised by dilatation and destruction of the bronchi caused by chronic infection or inflammation
52
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
53
differentials for diabetic retinopathy
macular degeneration vitreous haemorrhage cataracts hypertensive retinopathy migraine TIA
54
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
55
investigations in Myasthenia
Anti cholinesterase receptor antibodies Anti MUSK antibodies TFTS emg CT chest to check for Thymoma FVC if acute
56
what could trigger a myasethenic crisis?
infection dehydration stress non compliance with medication trauma anaemia drugs
57
name some types of muscular dystrophies
-myotonic dystrophy -limb-girdle muscular dystrophy -Duchennes muscular dystrophy/beckers -facioscapulohumeral dystrophy
58
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)
59
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
60
early signs of Parkinson's
constipation trouble sleeping falls tremor
61
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
62
Diagnosis of PD
clinical diagnosis Structural brain imaging to rule out other causes EG stroke/ NPH / SOL/ parkinsons plus syndromes
63
triad of Parkinsonism
Resting tremor Bradykinesia Rigidity
64
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
65
How to describe the movement of hands in PD
reduction in frequency and amplitude of movements
66
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
67
a cushingoid appearance...
moon shape facies abdominal straie aganthosis nigricans thinning of the arms and legs central adiposity gynaecomastia buffalo hump thin skin bruising
68
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
69
Function of the spleen
Filtration of the blood Iron metabolism Extra medullary haematopoesis Storage of RBCs and platelets
70
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
71
What do you see on fundoscopy for retinitis pigmentosa?
Pigmentary bony spicules
72
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)

PACES ellen (2 decks)

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