can only be diagnosed if psoriasis is present (F) also if fhx of psoriasis ref K&C

Other associations during active phase

Conjunctivitis

Iritis

Episleritis

Mouth ulcers

Fatty liver

Liver abscess/Portal pyaemia

Mesenteric or portal vein thrombosis

Venous thrombosis

Arthralgia

Erythema nodosum

Pyoderma gangrenosum

Associations unrelated to disease activity

Autoimmune hepatitis

Sclerosing cholangitis and cholangiocarcinoma (UC)

Gallstones

Renal amyloidosis and oxalate calculi

Sacroileitis/Ankylosing spondylitis (Crohn’s with HLA-B27)

Metabolic bone disease
92.Case history: male, heavy smoker, weight loss, cough, presents with weakness of quadriceps and anterior tibial muscles, absent knee and ankle jerk, flexor plantar responses, sensory loss in the saddle area, poor anal tone and weakness of knee extension. The likely diagnosis is:

a.Transverse myelitis F

b.S.A.C.D.C. F

c.Radiculoneuropathy F

d.Conus of the cord F

e.Lesion of the cauda equine T

Inflammatory demyelinating disorder. Often flu like illness preceeding. In some patients it’s the first manifestation of MS. Acute/subacute paraparesis. It’s a flaccid paralysis so weakness and loss of reflexes. Ascending sensory level loss doesn’t fit above case.

Subacute combined degeneration of the cord. Due to B12 deficiency. Absent ankle jerks due to neuropathy. Knee jerks may be absent or exaggerated due to cord lesion. Extensor plantar due to cord disease (UMN). Loss of vibration and proprioception due to involvement of the posterior columns. Sensory loss less common and mild. Saddle anaesthesia doesn’t fit

Radiculoneuropathy. Disorder of nerve roots. Due to compressive lesions eg. Disc prolapse or tumours. L3, L4 Knee extension. Saddle area S3, 4, 5. Doesn’t fit

Conus causes extensor plantar response plus absent knee and ankle jerks and altered saddle sensation

Cauda Equina. Saddle anaesthesia. Decreased anal tone. Difficulty urinating. Progressive motor weakness/Gait disturbance. Sensory level. Flaccid and areflexic. Flexor plantar. Causes: Canal stenosis. Lumbosacral nerve lesions. Secondary malignancy (Breast, LUNG, PROSTATE)
In the valvular disease of the aortic valve

1. 
   The least common congenital abnormality is bicuspid valve F
   
2. 
   The more severe the stenosis becomes, the louder the murmur becomes T
   
3. 
   The aortic valve is at risk of bacterial endocarditis T
   
4. 
   The most likely cause of significant stenosis is rheumatic fever in early life F
   
5. 
   Sudden death may occur in aortic stenosis T
   

1. 
   Most common
   
2. 
   Narrower opening means increased turbulence and therefore louder murmur. This is clinically unreliable. Murmur also gets shorter with increasing stenosis because greater pressures need to be generated to create blood flow.
   
3. 
   All valves at risk. BE in aortic valve results in valve damage and rergurg in some cases
   
4. 
   Most likely causes are senile degenerative and calcification of bicuspid valve. Rheumatic fever is a cause but not the most likely.
   
5. 
   Sudden death is rare but is more likely if other symptoms of stenosis have been prominent for a while.
   

Which of the following are true of chest pain within the last 6 hours

a. A man presenting with chest pain, less than 15 minutes duration, pressing pain, with normal ECG can be assured it is non-cardiac in origin F

b.A man presenting with chest pain, 30 minutes, pressing pain, radiating to

jaw and arm, with ST elevation on ECG, needs to be admitted to coronary care unit with view to thrombolysis T

c. A man presents with chest pain, 30 seconds, pressing pain, with ST elevation on ECG, needs to be admitted to coronary care unit and given prophylactic lidocaine F

4. 
   He needs hospital admission F
   

1. 
   This is a good plan if you don’t mind having your ass sued when he keels over and dies on the way out the door. Could be angina or loads of other stuff.
   
2. 
   More than 20 min suggest MI rather than angina. Morphine, Oxygen, Apsirin, Nitrates first. Thrombolysis is indicated for ST elevation MI. Prevents progression to Q wave transmural MI. Not indicated for non ST elevation eg. ST depression or T wave inversion.
   
3. 
   Lidocaine is given post MI to prevent ventricular arrhythmias. Not entirely certain he needs this after his 30 sec of chest pain but up to 30% of MIs are painless. Anyway it is not shown to reduce mortality when used prophylactically. (BNF P83)
   
4. 
   It depends on the history. I’d say no
   

Myelofibrosis is characterized by:

a.Increased B12 F

b.Often unproductive marrow aspirate T

c.Decreased neutrophil alkaline phosphatase

d.Leukoerythroblastic anemia T

e.Folate deficiency is common T

1. 
   Can’t find a reference to it so assuming its false
   
2. 
   The marrow is initially hypercellular with excess megakaryocytes. They release growth factor which results in proliferation of fibroblasts. Fibrosis makes it difficult to aspirate anything. They use a trephine biopsy instead.
   
3. 
   .
   
4. 
   Immature cells on blood film Reticulocytes and nucleated red cells and granulocyte precursors. Also tear drop poilikocytes and giant platelets
   
5. 
   Due to increased cell breakdown. Need supplementation
   

Marrow fibrosis, extramedullary hematopoiesis, Large spleen. White cell and platelet count can be low to high. Usually high at diagnosis (Soooo Helpful!) Urate high

Presents with lassitude, weight loss and night sweats. Age over 50

96The following are true of duodenal ulcer

a.Relapse rate is higher with campylobacter colonization F

b.H2 blockers are only used short term F

c.High dose antacids may heal ulcers F

d.H2 blockers have been superceded by oxyprenolone F

1. 
   Couldn’t find any info on it so assuming it’s false
   
2. 
   PPIs are preferred for long term use but there is technically nothing to stop the use of H2 blockers long term.
   
3. 
   According to the BNF liquid magnesium-aluminium antacids promote healing but less well than antisecretory drugs. Other books say antacids are crap and don’t heal ulcers. Prof Quigley said they don’t heal ulcers in his lecture so going with him on this one.
   
4. 
   What in the name of god is oxyprenolone. Its not in the BNF so going with false. I would say true if the said PPI
   

97The following are characterized by pustules

a.Psoriasis vulgaris T

b.Rosacea T

c.DLE F

d.Dermatitis herpetiformis F

e.Erythema marginatum F

1. 
   If psoriasis vulgaris is the same thing as pustular psoriasis then this is true. 2 types. Generalised is very severe with swinging pyrexia. Localised affects palms and soles.
   
2. 
   Characterised by a papulopustular rash on cheeks, centre of forehead and chin. Treated with oral tetracycline
   
3. 
   Discoid lupus characterized by hyperkeratosis and follicular plugging. May cause scarring alopecia.
   
4. 
   Intensely itchy blisters over extensor surfaces of limbs and over the back. Linear IgA deposition at the dermoepidermal junction.
   
5. 
   Starts as red macules which fade at the centre but remain red at the edges. Associated with rheumatis fever.
   

98The following are worsened by sunlight

a.Vitiligo T

b.Rosacea F

c.DLE F

d.Psoriasis vulgaris F

e.Seborrheic dermatitis F

1. 
   Sunburn or trauma may precipitate. Melanocytes present but abnormal production of melanin.
   
2. 
   Photosensitivity is a differential but can’t find anything to say it’s a trigger
   
3. 
   Butterfly rash is photosensitive but not the discoid lupus as far as I can tell.
   
4. 
   Well UV light used in treatment so probably not.
   
5. 
   Caused by pityrosporum ovale infection. Can’t find a reference to it being worsened by sunlight
   

99The following are true of HLA-DR3

a.It is most specific for Graves disease ?

b.It is of no value for connective tissue disorders F

c.It is characteristic of celiac disease F

d.It increased the relative risk of IDDM T

e.It is associated with NIDDM F
A) HLA B8, DR 2 or DR 3. It is associated but is it the most specific?

B) HLA B8, DR2 or DR3 in SLE

C) HLA DQ2

D) HLA DR 3 and or 4

E) Can’t find a reference to HLA involvement in Type 2

100Myotonic dystrophy is characterized by

a.facial weakness T

b.frontal baldness T

c.cataract T

d.hypertrophic sternomastoids F

e.proximal muscle weakness F

1. 
   Temporalis, Facial muscles, Sternomastoid
   
2. 
   And C) True but don’t know why.
   

D) Muscle wasting

E) Classically distal muscles

Autosomal dominant. Trinucleotide repeat on chr 19. Other features: Atrophy of testes and ovaries, cardiomyopathy, mild endocrine abnormalities and mental impairment. Die in middle age of intercurrent illness.

101Bloody diarrhea is characteristic of

a.Cholera F

b.Enteric (typhoid) fever F

c.Amoebic dysentery T

d.Schistosomiasis mansoni T

e.Tropical sprue F

1. 
   Severe painless diarrhea succeeded by vomiting. Then rice water diarrhea when normal gut content has been passed. Enormous fluid loss accompanied by cramps. No blood.
   
2. 
   1^st week fever, headache, myalgia, relative bradycardia, constipation, (diarrhea and vomiting in children) End of first week rose spots on the trunk, splenomegaly, ab distension, diarhoea, cough and epistaxis. Then bronchitis, delirium and other complactions coma and death if untreated. No reference to bloody diarrhea.
   
3. 
   Diarrhoea alternating with constipation. Sometimes mucus and streaks of blood. Offensive stool odour. May be tenderness along the line of the colon.
   
4. 
   Malaise, ab pain, frequent stools with blood stained mucus. May be hepatosplenomegaly.
   
5. 
   Chronic progressive malabsorption. PC Diarrhoea, ab distension, anorexia, fatigue, wgt loss. No reference to bloody diarrhoea
   

Causes of bloody diarrhea

Campylobacter

Shigella

Non typhoidal salmonellae

Enteroinvasive e coli

Enterohaemorrhagic e coli

Clostridium difficile

Vibrio parahaemolyticus

Entamoeba histolytica

Diverticular disease

Rectal or colonic malignancy

IBD

Bleeding haemorrhoids

Anal fissure

Ischaemic colitis

Intussusception

102The following are associated with normal small bowel villous appearances on biopsy

a.Gluten sensitive enteropathy F

b.Irritable bowel syndrome T

c.Post-gastrectomy steatorrhea T

d.Tropical sprue F

e.Pyloric stenosis T

Causes of subtotal villous atrophy

Coeliac, Tropical sprue, Dermatitis herpetiformis, Lymphoma, AIDS enteropathy, Giardiasis, Hypogammaglobulinaemia, Radiation, Whipples, Zollinger ellison

1. 
   Subtotal villous atrophy with marked inflammatory infiltrate.
   
2. 
   Normal histology. All other investigations normal also.
   
3. 
   Steatorrhoea due to enzyme loss?
   
4.