dpd Flashcards
A 50 y/o man presents w/ dyspepsia + weight loss. Ix: Hb 70; MCV 70. What test would you request?
- Abdominal CT
- Abdominal USS
- Erect CXR
- Colonoscopy
- OGD (Gastroscopy)
OGD as the symptoms suggest upper GI due to microcytic anaemia + dyspepsia (impaired digestion) + weight loss (red flag). If NAD then do colonoscopy.
Erect CXR done if there is perforation - pt will present w/ diffused abdo pain, rigidity, guarding, same w/ abdo CT
Abdo USS - next Ix in patients w/ deranged LFTs (common bile ducts to look for obstruction)
What Ix would you do if you found microcytic anaemia? (x 3)
OGD + Colonscopy: investigate top + tail; when to do which depends on upper/lower GI symptoms Haematinics: iron studies, ferritin, folate/B12 Coeliac screen (TTG ab + duodenal biopsy - this is diagnostic)
What kind of protein is ferritin and when will it be raised
Ferritin is an acute phase protein and will be raised in infection, inflammation + malignancy therefore iron deficiency anaemia + pneumonia may have normal ferritin as it is induced by infection.
what kind of protein is folate and when will it be raised
Folate is an acute phase protein. Infection + malignancy will cause increased folate
what confirms coeliac dis dx + what will be seen
Duodenal biopsy
Villous atrophy, crypt hyperplasia
What is coeliac disease?
Systemic AI disease triggered by dietary gluten peptides found in wheat, rye, barley + related grains.
Presentation: diarrhoea, bloating, abdo pain/discomfort, failure to thrive, iron deficiency microcytic anaemia, osteoporosis, dermatitis herpetiformis
tx for coeliac disease
Strict, lifelong gluten-free diet
Vit D supplements for vit D deficiency
A 70 y/o man presents w/ bloody diarrhoea. Stool micro + culture -ve. Stool C. diff toxin: -ve. What is the most likely diagnosis?
- Infective colitis
- Ischaemic colitis
- UC
- Appendicitis
- Gastroenteritis
Ischaemic colitis - typically older patients affecting smaller vessels as opposed to mesenteric ischaemia
Unlikely to be infective colitis due to -ve stool culture + -ve toxin.
UC typically younger patients (30-40s).
What are the 5 organisms that most commonly cause infective colitis therefore bloody diarrhoea?
CHESS organisms Campylobacter Haemorrhagic E. coli (0157) - assoc. w/ haemolytic uraemic syndrome Entomoaeba histolytica Salmonella Shigella
A 40 y/o man presents w/ palpitations that started 4 hours ago. ECG: AF. How would you treat him?
- Adenosine
- Amiodarone
- Digoxin
- Metoprolol
- DC cardioversion
- DC cardioversion as he is presenting < 48 hours
- Adenosine is for SVT
- Amiodarone is for broad complex tachycardia (VT) but works on all arrhythmias (often 2nd/3rd line); digoxin + metoprolol is for rate control
what is mx of AF that is <48h onset
DC cardioversion to revert back to SR or chemical cardioversion with flecainide
what is mx of AF that is >48h onset
Anticoagulate w/ LMWH + rate control with BB/digoxin
After 3-4 weeks, DC cardioversion to prevent clot dislodging
A sign is seen on a pt’s abdomen - the direction of flow in the veins below the umbilicus is towards the legs. What is the name of this clinical sign?
- Trousseau’s sign
- Virchow’s node
- Caput medusa
- Troisier’s sign
- Grey Turner sign
Caput medusa
= sign of portal hypertension
What does Trousseau’s sign indicate?
HIGH CALCIUM / hypercalcaemia
-carpopedal spasm with BP cuff on
OR
sign of thrombophlebitis in pancreatic C
virchows node indicates what
supraclavicular LN indicates gastric cancer
troisiers sign indicates what
enlargement of left supraclavicular LN due to secondary involvement
grey turners sign indicates what
bruising on flanks associated with pancreatitis (retroperitoneal haemorrhage)
A 20 y/o boy presents w/ recent diarrhoea + malaise. Hb 70; Cr 300. Arrows on blood film point to fragmented cells. What does this indicate?
- Codocytes
- Eliptocytes
- Lymphocytes
- Schistocyte
- Spherocyte
Schistocyte - red cell fragment Not codocyte (target cell) seen in hyposplenism
What are the signs of portal hypertension?
Presents w/ signs of decompensated liver disease: Encephalopathy Ascites SBP Variceal bleed
What is the pathophysiology in MAHA?
Lots of tiny clots in small vessels (microangiopathic) which narrow small vessels. As RBCs pass through these narrow vessels they break up –> haemolysis.
This is why you see schistocytes in MAHA + low Hb
What is the pathophysiology in DIC?
Widespread intravascular coagulation - constant making and breaking of clots.
Paradoxically prone to bleeding as clotting factors being used up
What are the levels of (1) platelets + fibrinogen (2) PT/APTT (3) D-Dimer/fibrin degradation products in DIC?
- Decreased platelets + fibrinogen as they used up to make tiny clots + fibrinogen is turned into fibrin as RBC trapped in fibrin strands
- Increased PT/APTT as clotting factors used up
- Increased D-dimer/fibrin degradation products due to fibrinolysis
Which part of the coagulation pathway does (1) PT and (2) APTT refer to?
- PT refers to the extrinsic pathway
2. APTT refers to the intrinsic pathway
How does Haemolytic Uraemic Syndrome present?
1.Haemolysis - decreased Hb and increased bilirubin causing pre-hepatic jaundice
2.Uraemia
3.Thrombocytopaenia = Decreased platelets
4.Abdo pain
Assoc. w/ E coli 0157 in children commonly