Passmed Flashcards
1
Q
What is schistomiasis
A
aka bilharzia - a parasitic flatwork infection
2
Q
what are the acute symptoms of schistosomiasis
A
swimmers itch
acute schistosomiasis syndrome (katayama fever- fever, urticaria/angioedema, arthralgia/myalgia, cough, diarrhoea, eosinophillia)
3
Q
what are the symptoms of chronic schistosomiasis
A
Schistosoma haematobium casuse chronic infection
the worms deposit egg clusters in the bladder, causing inflammation.
Calcification seen on x-ray is calcification of the egg clusters
They can cause obstructive uropathy and damage to the kidney
features: frequency, haematuria and bladder calcification
4
Q
how is schistosomiasis diagnosed?
A
Antibodies
urine or stool microscopy looking for eggs
5
Q
how is Schistosomiasis managed
A
single oral dose of praziquantel
6
Q
which type of Schistosoma can cause liver cirrhosis, variceal disease and cor pulmonalse
A
Schistoma mansoni and Schistosoma japonicum
These worms mature in the liver and then travel through the portal system to inhabit the distal colon. Their presence in the portal system can lead to progressive hepatomegaly and splenomegaly due to portal vein congestion.
7
Q
What on biopsy from OGD suggests gastric adenocarcinoma ?
A
signet ring cells
8
Q
what are the risk factors for gastric cancer?
A
H.pylori (triggers inflammation of the mucosa which leads to atrophy and intestinal metaplasia)
Atrophic gastritis
diet (salt and salt-preserved foods, nitrates)
smoking
blood group
9
Q
what are they symptoms of gastric cancer ?
A
abdominal pain (vague, epigastric, dyspepsia)
weight loss
N&V
dysphagia
GI bleeding
supraclavicular lymph node (Virchow’s node)
periumbilical nodule (sister Mary Joeseph’s node )
10
Q
Investigations for gastric cancer
A
OGD + Biopsy - sinet ring cells may be seen (they contain a large vacuole of mucin which displaces the nucleus to one side) Higher number of signet ring cells are associated with a worse prognosis
Staging CT
11
Q
management of gastric cancer
A
surgery (endoscopic mucosal resection, partial gastrectomy, total gastrectomy)
chemotherapy
12
Q
what causes farmers lung
A
Saccharopolyspora rectivigula
Contaminated hay is the most common source of it
13
Q
what is extrinsic allergic alveolitis?
A
AKA hypersensitivity pneumonitis
A condition caused by hypersensitivity-induced lung damage due to a variety of inhaled organic particles.
It is largely caused by immune-complex mediated tissue dame (type III hypersensitivity), although delayed hypersensitivity (type IV) is also thought to play a role in EAA, especially in chronic phase)
14
Q
what are examples of extrinsic allergic alveolitis?
A
Burd fanciers’ lung - avian proteins from bird droppings
farmers lung - spores of Saccharopolyspora rectivirgula from wet hay (formerly Micropolyspora faeni)
malt workers’ lung - aspergillus clavatus
mushroom workers’ lung - thermophilic actinomycetes
15
Q
How does EAA present?
A
Acute (4-8 hours after exposure) dyspnoea, dry cough, fever
Chronic (occurs weeks-months after exposure)
lethargy, dyspnoea, productive cough, anorexia, weight loss
16
Q
what are the investigations for EAA?
A
Imaging (upper/mid-zone fibrosis)
Bronchoalveolar lavage - lymphocytosis
serologic assays for specific IgG antibodies
Blood - NO oesinosphilla
17
Q
Management of EAA
A
avoid precipitating factors
oral glucocorticoids
18
Q
what are the features of SPB?
A
ascites, abdominal pain, gever
19
Q
how is SPB diagnosed?
A
neutrophil count > 250 cells/ul
most common organism found is E.coli
20
Q
what is the management of SPB?
A
IV cefotaxime
21
Q
who gets SPB prophylaxis and what is the Abx of choice
A
patients who have previously had an episode of SPB
patients with fluid protein <15d/l and either Child-Pugh score of at least 9 or hepatorenal syndrome
Offer prophylactic oral ciprofloxacin or norfloxacin
22
Q
what are the features that suggest primary hyperaldosteronism?
A
Hypertension
Hypokalaemia
mild alkalosis (raised bicarbonate)
23
Q
What can excessive ACTH secretion cause?
A
hyperaldosteronism
elevated glucocorticoid activity
24
Q
what is the most common cause of primary hyperaldosteronism?
A
Bilateral adrenal hyperplasia
It used to be thought that an adrenal adenoma (Conn’s)
Differentiating between the two is important as this determines the treatment.
Adrenal carcinoma is an extremely rare cause of primary hyperaldosteronism
25
what are the investigations for primary hyperaldosteronism?
a plasma aldosterone/renin ratio is the first line investigation (should show high aldosterone levels alongside low renin levels - negative feedback due to sodium retention from aldosterone)
Following this a a CT abdo and adrenal vein sampling used to differentiate unilateral and bilateral sources of aldosterone
26
how is primary hyperaldosteronsism managed?
adrenal adenoma: surgery
bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone
27
Autosomal recessive conditions ve autosomal dominant conditions
Autosomal recessive conditions are 'metabolic' - exceptions: inherited ataxias
Autosomal dominant conditions are 'structural' - exceptions: Gilbert's, hyperlipidaemia type II
28
what should be used to treat eclampsia whilst the delivery plan is made
what needs to be monitored whilst giving this treatment
magnesium sulphate
monitor respiratory rate
also urine output, reflexes and oxygen saturation
** calcium gluconate is the first-line treatment for magnesium sulphate-induced respiratory depression
29
what are the causes of riased prolactin
pregnancy
prolactinoma
physiological
polycystic ovarian syndrome
primary hypothyroidism
phenothiazines, metoclopramide, domperidone
30
what are the features of raised prolactin
men: impotence, loss of libido, galactorrhoea
women: amenorrhoea, galactorrhoea
31
what skin disorder is associated with gastric cancer?
Acanthosis nigricans
32
what skin condition is associated with lymphoma?
Acquired ichthyosis
erythroderma
33
what skin condition is associated with gastrointestinal and lung cancer?
Acquired hypertrichosis lanuginosa
34
what skin condition is associated with ovarian and lung cancer?
Dermatomyositis
35
what is erythema gyratum rapens associated with?
lung cancer
36
what malignancy is associated with migratory thrombophlebitis?
pancreatic cancer
37
what malignancy is associated with glucagonoma?
Necrolytic migratory erythema
38
what is pyoderma gangrenosum associated with?
myeloproloferative disorders
39
what is sweet's syndrome associated with?
Haematological malignancy e.g. Myelodysplasia - tender, purple plaques
40
what is tylosis associated with?
oesophageal cancer
41
what are the features of SVC obstruction?
dyspnoea is the most common symptom
swelling of the face, neck and arms - conjunctival and periorbital oedema may be seen
headache: often worse in the mornings
visual disturbance
pulseless jugular venous distension
42
what are the causes of SVC obstruction?
common malignancies: small cell lung cancer, lymphoma
other malignancies: metastatic seminoma, Kaposi's sarcoma, breast cancer
aortic aneurysm
mediastinal fibrosis
goitre
SVC thrombosis
43
what is the treatment of cluster headache?
100% oxygen and SC triptan
prophylaxis - verapamil
44
what is PCI
Percutaneous coronary intervention (PCI) is a technique used to restore myocardial perfusion in patients with ischaemic heart disease, both in patients with stable angina and acute coronary syndromes. Stents are implanted in around 95% of patients - it is now rare for just balloon angioplasty to be performed
45
what are the different typyes of stent used in PCI
bare-metal stent (BMS)
drug-eluting stents (DES): stent coated with paclitaxel or rapamycin which inhibit local tissue growth. Whilst this reduces restenosis rates the stent thrombosis rates are increased as the process of stent endothelisation is slowed
46
what medication should be given post PCI stent insertion?
he most important factor in preventing stent thrombosis is antiplatelet therapy. Aspirin should be continued indefinitely.
47
complications of PCI
bleeding
retroperitoneal haematoma
femoral pseudoaneurysm
cholesterol embolisation (occurs due to embolisation of cholesterol released from atherosclerotic plaques, purpura, livedo reticularis, renal impairment, blue toes
Long term complications - restenosis, stent thrombosis
48
what HLA is haemochromatosis associated with
HLA-A3
49
What HLA is bechet's disease associated with
HLA-B51
50
What conditions is HLA B27 associated with?
ankylosing spondylitis
reactive arthritis
acute anterior uveitis
51
what HLA is coeliac disease associated with
HLA DQ2/DQ8
52
what conditions is HLA-DR2 associated with
narcoplepsy
good pastures
53
what conditions is HLA DR3 associated with?
Dermatitis herpetiformis
Sjogren's syndrome
primary biliary cirrhosis
54
what conditions is HLA-DR$ associated with ?
type 1 diabetes
RA (in particular the DRB1 gene)
55
what chromosome is HLA antigen encoded by
6
56
when suspecting SAH at what point can LP be done?
12 hours after the onset of headache
57
what is the treatment for toxoplasmosis?
If they are immunocompetent - they don't usually require treatment
supportive care with fluids and analgesia - most infections are self limiting.
If there is eye involvement - toxoplasma chorioretinitis and those who are immunosuprresed - a combination of pyrimethamine and sulfadiazine is usually given for several weeks.
58
what kind of bacteria is toxoplasmosis?
protozoan
59
how do you get infected with toxoplasmosis?
via the gastrointestinal tract, lung or broken skin. It's oocysts release trophozoites which migrate widely around the body including to the eye, brain and muscle.
60
what are the symptoms of cerebral toxoplasmosis?
headache
confusion
drowsiness
61
what would a CT show in cerebral toxoplasmosis?
single or mutiple ring-enhancing lesions, mass effect may be seen
62
what can congenital toxoplasmosis cause
neurological damage- cerebral calcification, hydrocephalus, chorioretinitis
ophthalmic damage- retinopathy, cataracts
63
which type of diabetic medication cause weight gain?
Sulfonlyureas cause weight gain (gliclazide)
64
what are the adverse effects of sulfonylureas?
hyponatraemia secondary to syndrome of inappropriate ADH secretion
bone marrow suppression
hepatotoxicity (typically cholestatic)
peripheral neuropathy
they should be avoided in pregnancy
65
what is sideroblastic anaemia
66
what is sideroblastic anaemia?
a condition where the red cells fail to completely for haem
This leads to deposits of iron in the mitochondria that form a ring around the nucleus called a ring sideroblast
it can be congenital or acquired
67
what are the causes of sideroblastic anaemia?
Congenital cause: delta-aminolevulinate synthase-2 deficiency
Acquired causes
myelodysplasia
alcohol
lead
anti-TB medications
68
how do you investigate sideroblastic anaemia?
full blood count - hypochromic, microcytic anaemia
iron studies - high ferritin, high iron, high transferrin saturation
blood film -basophilic strpplinf of RBC
Bone marrow - prussian blue (also known as perls stain) will show ringed sideroblasts
69
what is HOCM?
How is HOCM inherited?
Hypertrophic obstructive cardiomyopathy (HOCM) is an autosomal dominant disorder of muscle tissue caused by defects in the genes encoding contractile proteins
70
what may you see on an ECG in a person with HOCM?
left ventricular hypertrophy
non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen
deep Q waves
atrial fibrillation may occasionally be seen
71
what are the characteristics of the heart in someone with HOCM?
predominantly diastolic dysfunction - left ventricular hypertrophy - decreased cmpliance - decreased cardiac output
Characterised by myofibrillar hypertrophy with chaotic and disorganised fashion myocytes
72
what are the features of HOCM?
often asymptomatic
exerional dyspnoea
angina
syncope (typically following exercise)
sudden death
jerk pulse, large a waves, double apex beat
systolic murmurs -ejection systolic murmur: due to left ventricular outflow tract obstruction. Increases with Valsalva manoeuvre and decreases on squatting
pansystolic murmur: due to systolic anterior motion of the mitral valve → mitral regurgitation
73
what arrhythmia are associated with HOCM
friedreich's ataxia
wolff parkinson white
74
what are the echo findings of HOCM ?
Echo findings - mnemonic - MR SAM ASH
mitral regurgitation (MR)
systolic anterior motion (SAM) of the anterior mitral valve leaflet
asymmetric hypertrophy (ASH)
75
what are the adverse effects of levodopa?
dyskinesia
'on-off' effect
postural hypotension
cardiac arrhythmias
nausea & vomiting
psychosis
reddish discolouration of urine upon standing
76
what is the key pathophysiological feature of metabolic syndrome?
insulin resistance
77
how long should you monitor someone after anaphylaxis?
6 hours
patients can have a biphasic reaction = this includes a recurrence of symptoms that develop after apparent resolution of the initial reaction
78
management of anaphylaxis
IM adrenaline (in adults 500mcg)
can be given every 5 minuites if needed
the best location for the IM injection is he anterolateral aspect of the middle third of the thigh
79
HLAs
SjogR3n's --> HLA-DR3
D3Rmatitis Herpetiformis --> HLA-DR3
Rheumatoid 4rthritis --> HLA-DR4
hA3mochromatosis --> HLA-A3
B5hcet's disease --> HLA-B51
coeliaQ Disease --> HLA-DQ2/DQ8 (only one with a Q)
naRcolepsy + GoodpastuRe's --> HLA-DR2 (2 R's)
Bones (seronegative arthritis, ankylosing spondylitis) --> HLA-B27 (letter B)
80
what drugs affect acetylator status?
isoniazid
procainamide
hydralazine
dapsone
sulfasalazine
81
what are drugs exhibiting zero-order kinetics?
phenytoin
salicylates (e.g. high-dose aspirin)
heparin
ethanol
82
what is complex regional pain syndrome?
Complex regional pain syndrome (CRPS) is a condition that causes severe, persistent pain and swelling, typically affecting one of the limbs. It usually develops after an injury, surgery, or fracture.
83
what in tumour necrosis factor?
Tumour necrosis factor (TNF) is a pro-inflammatory cytokine with multiple roles in the immune system. It is secreted mainly by macrophages
84
what are the effects of tumour necrosis factor on the immune system?
activates macrophages and neutrophils
acts as costimulator for T cell activation
key mediator of bodies response to Gram negative septicaemia
similar properties to IL-1
anti-tumour effect (e.g. phospholipase activation)
85
what are examples of TNF inhibitors?
Examples of TNF inhibitors
infliximab: monoclonal antibody, IV administration
etanercept: fusion protein that mimics the inhibitory effects of naturally occurring soluble TNF receptors, subcutaneous administration
adalimumab: monoclonal antibody, subcutaneous administration
golimumab: subcutaneous administration
adverse effects of TNF blockers include reactivation of latent tuberculosis and demyelination
86
features of anti phospholipid syndrome
venous/arterial thrombosis
recurrent miscarriage
Lived reticular
pre-eclampsia, pulmonary hypertension
thrombocytopenia
prolonged APTT
Antibodies - anticardiolipin, anti-beta2 glycoprotein I (anti-bata2GPI) antibodies, lupus anticoagulant
87
which type of thyroid cancer is associated with hashimoto/autoimmune thyroiditis
thyroid lymphoma
88
what are contraindications to the TB vaccine?
previous BCG vaccination
a past history of tuberculosis
HIV
pregnancy
positive tuberculin test (Heaf or Mantoux)
89
what is the mechanism of action of mycophenolate?
Mycophenolate mofetil (MMF) reduces lymphocyte production through inhibition of iosine-5'-monophosphate dehydrogenase which is needed for purine synthesis
90
what is the most common cause of bladder calcification world wide?
Schistosomiasis
91
What is schistomosoma haematobium?
how is it managed?
These worms deposit egg clusters (pseudopapillomas) in the bladder, causing inflammation. The calcification seen on x-ray is actually calcification of the egg clusters, not the bladder itself.
single dose of praziquantel
92
what ate the adverse effects of Bisphosphonates?
oesophageal reactions: oesophagitis, oesophageal ulcers (especially alendronate)
osteonecrosis of the jaw
increased risk of atypical stress fractures of the proximal femoral shaft in patients taking alendronate
acute phase response - fever, myalgia and arthralgia
hypocalcaemia
93
How do you council a patient to take bisphosphonates?
Tablets should be swallowed whole with plenty of water while sitting or standing; to be given on an empty stomach at least 30 minutes before breakfast (or another oral medication); patient should stand or sit upright for at least 30 minutes after taking tablet'
94
What is Diabetes Insipidus?
Diabetes insipidus (DI) is a condition characterised by either a decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI).
95
Investigations for diabetes insipidus?
high plasma osmolality, low urine osmolality
a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
water deprivation test
96
Managament of Diabetes insipidus?
nephrogenic diabetes insipidus
thiazides
low salt/protein diet
central diabetes insipidus can be treated with desmopressin
97
What are angiod retinal streaks?
Angioid retinal streaks are seen on fundoscopy as irregular dark red streaks radiating from the optic nerve head. They are caused by degeneration, calcification and breaks in Bruch's membrane .
98
Causes of angiod retinal streaks?
pseudoxanthoma elasticum
Ehler-Danlos syndrome
Paget's disease
sickle-cell anaemia
acromegaly
99
What is Heredtary angioedema?
autosomal dominant condition associated with low plasma levels of the C1 inhibitor (C1-INH, C1 esterase inhibitor) protein.
C1-INH is a multifunctional serine protease inhibitor - the probable mechanism behind attacks is uncontrolled release of bradykinin resulting in oedema of tissues.
100
Symptoms of hereditary angioedema?
attacks may be proceeded by painful macular rash
painless, non-pruritic swelling of subcutaneous/submucosal tissues
may affect upper airways, skin or abdominal organs (can occasionally present as abdominal pain due to visceral oedema)
urticaria is not usually a feature
101
Management of hereditary angioedema?
acute
HAE does not respond to adrenaline, antihistamines, or glucocorticoids
IV C1-inhibitor concentrate, fresh frozen plasma (FFP) if this is not available
prophylaxis: anabolic steroid Danazol may help
102
What types of cancer can asbestos cause?
bronchial carcinoma as well as mesothelioma
103
Common carcinogens?
104
what is calciphylaxis?
Calciphylaxis is a rare complication of end-stage renal failure. The underlying mechanism is not clear, however it results in deposition of calcium within arterioles causing microvascular occlusion and necrosis of the supplied tissue. It most commonly affects the skin and presents with painful necrotic skin lesions.
105
what is the site of action of ADH?
Collecting ducts
106
T2DM diagnosis?
If the patient is symptomatic:
fasting glucose greater than or equal to 7.0 mmol/l
random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)
If asymptomatic - the above apply but must be demonstrated on 2 separate occasions
a HbA1c of greater than or equal to 48 mmol/mol (6.5%) is diagnostic of diabetes mellitus
## Footnote
a HbAlc value of less than 48 mmol/mol (6.5%) does not exclude diabetes (i.e. it is not as sensitive as fasting samples for detecting diabetes)
107
What conditions may HbA1c not be used for diagnosis?
haemoglobinopathies
haemolytic anaemia
untreated iron deficiency anaemia
suspected gestational diabetes
children
HIV
chronic kidney disease
people taking medication that may cause hyperglycaemia (for example corticosteroids)
108
What is impaired fasting glucose?
A fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l implies impaired fasting glucose (IFG)
Impaired glucose tolerance (IGT) is defined as fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l
## Footnote
Diabetes UK suggests:
'People with IFG should then be offered an oral glucose tolerance test to rule out a diagnosis of diabetes. A result below 11.1 mmol/l but above 7.8 mmol/l indicates that the person doesn't have diabetes but does have IGT.'
109
Clincial features of Ectasy poisoning?
Clinical features
neurological: agitation, anxiety, confusion, ataxia
cardiovascular: tachycardia, hypertension
hyponatraemia
this may result from either syndrome of inappropriate ADH secretion or excessive water consumption whilst taking MDMA
hyperthermia
rhabdomyolysis
110
Management of Ectasy poisoning?
supportive
dantrolene may be used for hyperthermia if simple measures fail
111
causes of primary hyperaldosteronism?
bilateral idiopathic adrenal hyperplasia: the cause of around 60-70% of cases
adrenal adenoma: 20-30% of cases
unilateral hyperplasia
familial hyperaldosteronism
adrenal carcinoma
112
Features of primary hyperaldosteronism?
hypertension
increasingly recognised but still underdiagnosed cause of hypertension
hypokalaemia
e.g. muscle weakness
this is a classical feature in exams but studies suggest this is seen in only 10-40% of patients, and is more common with adrenal adenomas
metabolic alkalosis
113
Investigations for primary hyperaldosteronism?
plasma aldosterone/renin ratio is the first-line investigation in suspected primary hyperaldosteronism
following this a high-resolution CT abdomen and adrenal vein sampling is used to differentiate between unilateral and bilateral sources of aldosterone excess
if the CT is normal adrenal venous sampling (AVS) can be used to distinguish between unilateral adenoma and bilateral hyperplasia
114
what would a aldosterone renin ratio show in primary hyperaldosteronism?
should show high aldosterone levels alongside low renin levels (negative feedback due to sodium retention from aldosterone)
115
Management of primary hyperaldosteronism?
adrenal adenoma: surgery (laparoscopic adrenalectomy)
bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone
116
Poor prognostic factors in CLL?
male sex
age > 70 years
lymphocyte count > 50
prolymphocytes comprising more than 10% of blood lymphocytes
lymphocyte doubling time < 12 months
raised LDH
CD38 expression positive
TP53 mutation
## Footnote
deletions of part of the short arm of chromosome 17 (del 17p) are seen in around 5-10% of patients and are associated with a poor prognosis
117
What is good prognostic factor in CLL?
deletion of the long arm of chromosome 13 (del 13q) is the most common abnormality, being seen in around 50% of patients. It is associated with a good prognosis
118
Pathophysiology of SLE?
Pathophysiology
autoimmune disease: SLE a type 3 hypersensitivity reaction
associated with HLA B8, DR2, DR3
thought to be caused by immune system dysregulation leading to immune complex formation
immune complex deposition can affect any organ including the skin, joints, kidneys and brain
119
What is pernicious anaemia?
Pernicious anaemia is an autoimmune disorder affecting the gastric mucosa that results in vitamin B12 deficiency
Pathophysiology
antibodies to intrinsic factor +/- gastric parietal cells
intrinsic factor antibodies → bind to intrinsic factor blocking the vitamin B12 binding site
gastric parietal cell antibodies → reduced acid production and atrophic gastritis. Reduced intrinsic factor production → reduced vitamin B12 absorption
vitamin B12 is important in both the production of blood cells and the myelination of nerves → megaloblastic anaemia and neuropathy
120
HHS diagnostic criteria
here are no precise diagnostic criteria but the following are typically seen
hypovolaemia
marked hyperglycaemia (>30 mmol/L)
significantly raised serum osmolarity (> 320 mosmol/kg)
can be calculated by: 2 * Na+ + glucose + urea
no significant hyperketonaemia (<3 mmol/L)
no significant acidosis (bicarbonate > 15 mmol/l or pH > 7.3 - acidosis can occur due to lactic acidosis or renal impairment)
121
Investigations for pernicious anaemia?
Investigation
full blood count
macrocytic anaemia: macrocytosis may be absent in around of 30% of patients
hypersegmented polymorphs on blood film
low WCC and platelets may also be seen
vitamin B12 and folate levels
a vitamin B12 level of >= 200 nh/L is generally considered to be normal
antibodies
anti intrinsic factor antibodies: sensivity is only 50% but highly specific for pernicious anaemia (95-100%)
anti gastric parietal cell antibodies in 90% but low specificity so often not useful clinically
122
what is the pathophysiology of diabetic retinopathy ?
Hyperglycaemia is thought to cause increased retinal blood flow and abnormal metabolism in the retinal vessel walls. This precipitates damage to endothelial cells and pericytes
Endothelial dysfunction leads to increased vascular permeability which causes the characteristic exudates seen on fundoscopy. Pericyte dysfunction predisposes to the formation of microaneurysms. Neovasculization is thought to be caused by the production of growth factors in response to retinal ischaemia
123
How is non-proliferative retinopahy classified?
Mild NPDR
1 or more microaneurysm
Moderate NPDR
microaneurysms
blot haemorrhages
hard exudates
cotton wool spots ('soft exudates' - represent areas of retinal infarction), venous beading/looping and intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR
Severe NPDR
blot haemorrhages and microaneurysms in 4 quadrants
venous beading in at least 2 quadrants
IRMA in at least 1 quadrant
124
What are the features of proliferative retinopathy?
retinal neovascularisation - may lead to vitrous haemorrhage
fibrous tissue forming anterior to retinal disc
more common in Type I DM, 50% blind in 5 years
125
What are the features of diabetic maculopathy?
based on location rather than severity, anything is potentially serious
hard exudates and other 'background' changes on macula
check visual acuity
more common in Type II DM
126
Management of diabetic maculopathy?
if there is a change in visual acuity then intravitreal vascular endothelial growth factor (VEGF) inhibitors
127
Management of non-proliferative diabetic retinopathy?
regular observation
if severe/very severe consider panretinal laser photocoagulation
128
management of proliferative diabetic retinopathy?
Panretinal laser photocoagulation
Intravitreal VEGF INHIBITORS (E.G. RANIBIZUMAB)
if severe or vitreous haemorrhage: vitreoretinal surgery
129
Complications of panretinal photocoagulation
following treatment around 50% of patients develop a noticeable reduction in their visual fields due to the scarring of peripheral retinal tissue
other complications include a decrease in night vision (rods are predominantly responsible for vision in low light conditions, the majority of rod cells are located in the peripheral retina), a generalised decrease in visual acuity and macular oedema
130
Mechanism of action of cyclophosphamide and side effets?
alkylating agent - causes cross linking in DNA
Adverse effects - haemorrhagic cystiis, myelosupression and transitional cell carcinoma
131
What is hemibalism?
Hemiballism occurs following damage to the subthalamic nucleus. Ballisic movements are involuntary, sudden, jerking movements which occur contralateral to the side of the lesion. The ballisic movements primarily affect the proximal limb musculature whilst the distal muscles may display more choreiform-like movements
Symptoms may decrease whilst the patient is asleep.
Antidopaminergic agents (e.g. Haloperidol) are the mainstay of treatment
132
What is the most common cause of thrombophilia?
factor V Leiden (activated protein C resistance): most common cause of thrombophilia
133
oral codeine to oral morphine
oral morphine to oxycodone
Codeine to morphone - devide by 10
morphine to oxycodone - devide by 1.5 to 2
134
Dermatitis herpatiformis?
Dermatitis herpetiformis is an autoimmune blistering skin disorder associated with coeliac disease. It is caused by deposition of IgA in the dermis.
135
features of dermatits herpatiformis?
itchy, vesicular skin lesions on the extensor surfaces (e.g. elbows, knees, buttocks)
136
Investigations and management of dermatitis herpatiformis?
Diagnosis
skin biopsy: direct immunofluorescence shows deposition of IgA in a granular pattern in the upper dermis
Management
gluten-free diet
dapsone
