Flashcards in Chemical Pathology Deck (64)
Which of the following clinical signs is the best indicator of hypovolaemia?
(b) Postural hypotension
(c) Reduced skin turgor
(e) Low urine Na+ (<20)
The correct answer is (e) Low urine Na+ (<20). All of these signs indicate hypovolaemia however some of them are better than others, and others require some context, or might be affected by confounding factors. However, low urine Na+ is a very accurate indicator that the patient is hypovolaemic as they are retaining salt.
Which of the following is a cause of hypovolaemic hyponatraemia?
(b) Cardiac failure
(d) Adrenal insufficiency
The correct answer is (e) Diuretics.
Hypothyroidism (a) and adrenal insufficiency (d) are causes of euvolaemic hyponatraemia.
Cardiac failure (b) and cirrhosis (c) are causes of hypervolaemic hyponatraemia.
Which of the following is not a cause of SIADH?
(b) Lung cancer
(d) Nephrotic syndrome
The correct answer is (d) nephrotic syndrome. Nephrotic syndrome is a cause of hypervolaemic hyponatraemia.
In a patient with SIADH what pattern would you expect?
(a) Low plasma osmolality, low urine osmolality.
(b) High plasma osmolality, low urine osmolality.
(c) Low plasma osmolality, high urine osmolality.
(d) High plasma osmolality, high urine osmolality.
(e) Mate I don't even know what osmolality is.
The correct answer is (c) Low plasma osmolality, high urine osmolality.
Due to SIADH you have excessive water retention, which initially creates volume expansion, which then stimulates atrial natriuretic peptide, which causes water and sodium loss through the kidneys. This is why SIADH causes a euvolaemic hyponatraemia.
Which of the following drugs can be used to treat SIADH?
The correct answer is (a) Demeclocycline.
Demeclocycline reduces responsiveness of collecting tubule cells to ADH, but U&Es must be monitored due to risk of nephrotoxicity.
Another drug that can be used is Tolvaptan which is a V2 receptor antagonist.
Opiates (b), Carbamazepine (c), PPIs (d) and TCAs (e) are all drugs that can cause SIADH.
What are the two main stimuli for ADH secretion?
(a) Reduced blood volume and reduced serum osmolality
(b) Reduced blood volume and increased serum osmolality
(c) Increased blood volume and reduced serum osmolality
(d) Increased blood volume and increased serum osmolality
The correct answer is (b) Reduced blood volume and increased serum osmolality.
State four causes of hyperkalaemia.
The main causes of hyperkalaemia can be broken down into four groups.
Renal impairment or disease which causes reduced renal excretion of potassium.
Drugs such as ACE inhibitors, ARBs and spironolactone which all act to reduce aldosterone which in turn prevent potassium excretion.
Low aldosterone due to Addison's disease or type 4 renal tubular acidosis (low renin, low aldesterone)
Potassium release from cells as in rhabdomylosis or acidosis.
Which of the following is the correct treatment regimen for hyperkalaemia?
(a) 50ml 10% calcium gluconate, 50 ml 50% dextrose and 10 units of insulin and nebulized salbutamol.
(b) 10ml 10% calcium gluconate, 10 ml 50% dextrose and 10 units of insulin and IV salbutamol.
(c) 50ml 10% calcium gluconate, 10 ml 50% dextrose and 5 units of insulin and nebulized salbutamol.
(d) 10ml 10% calcium gluconate, 50 ml 50% dextrose and 10 units of insulin and nebulized salbutamol.
(e) 10ml 10% calcium gluconate, 50 ml 50% dextrose and 5 units of insulin and IV salbutamol.
The correct answer is (d) 10ml 10% calcium gluconate, 50 ml 50% dextrose and 10 units of insulin and nebulized salbutamol.
Although this is the initial emergency treatment of hyperkalaemia, the full treatment would be to also treat the underlying cause of the hyperkalaemia.
Hypokalaemia is a side effect of which of the following drugs?
The correct answer is (a) Furosemide.
All of the other options cause hyperkalaemia.
67 year old man presents with D&V for the past 2 days and was started on bendroflumethiazide for hypertension 2 weeks previously. He has dry mucous membranes and reduced skin turgor. Na+ is 129, K+ 3.5, Urea 8.0 and Creatinine 100.
What is this patient's status and what should the management be?
(a) Euvolaemic hyponatraemia so treat with hypertonic saline.
(b) Hypervolaemic hyponatraemia so treat with fluid restriction and 0.9% saline.
(c) Hypovolaemic hyponatraemia so treat with hypertonic saline
(d) Hypovolaemic hyponatraemia, but it's not too low so conservatively watch and wait and encourage the patient to eat and drink
(e) Hypovolaemic hyponatraemia so volume replacement with 0.9% saline.
The correct answer is (e) Hypovolaemic hyponatraemia so volume replacement with 0.9% saline.
This patient has three separate causes of hypovolaemic hyponatraemia in diarrhoea, vomiting and diuretic.
55 year old man presents with jaundice and a past history of excessive alcohol intake. He has multiple spider naevi, shifting dullness and splenomegaly. Na+ 122, K+ 3.5, Urea 2.0 and Creatinine 80.
What is this patient's status and what should the management be?
(a) Euvolaemic hyponatraemia so give normal saline and treat the underlying cause.
(b) Hypovolaemic hyponatraemia so give normal saline and treat the underlying cause.
(c) Hypervolaemic hyponatraemia so treat with fluid restriction, hypertonic saline, and treat the underlying cause.
(d) Hypervolaemic hyponatraemia so give normal saline and treat the underlying cause.
(e) Hypervolaemic hyponatraemia so treat with fluid restriction and treat the underlying cause.
The correct answer is (e) Hypervolaemic hyponatraemia so treat with fluid restriction and treat the underlying cause.
This patient has cirrhosis which is a cause of hypervolaemic hyponatraemia. Cirrhosis causes excess NO production which leads to vasodilation, which causes a drop in blood pressure which in turns stimulates ADH release and subsequent fluid retention and a dilutional hyponatraemia.
What occurs first in response to hypoglycaemia?
(a) Suppression of insulin
(b) Release of glucagon
(c) Release of adrenaline
(d) Release of cortisol
(e) Release of insulin
The correct answer is (c) release of adrenaline.
(a) Is the cleavage product of insulin
(b) Is secreted in equimolar amounts to insulin
(c) Has a half life of 2 hours
(d) Interferes with insulin management
(e) All of the above
The correct answer is (b), C-peptide is secreted in equimolar amounts to insulin.
Pro-insulin is cleaved to give C-peptide and insulin so (a) is wrong.
The half life of C-peptide is about 30 minutes so (c) is wrong.
20 year old female, BMI 17kg/m2, with some Lanugo hair noted. Finger prick glucose was 3.8mmol/L, and routine bloods were taken. Doctor rung by lab 1 hour later as plasma glucose was 2.6mmol/L.
What is the cause of her low blood sugar?
(a) Undertakes strenuous exercise regularly
(c) Anorexia with poor liver glycogen stores
(d) Laxative abuse
(e) Zollinger-Ellison syndrome
The correct answer is (c) anorexia with poor liver glycogen stores.
The finger prick glucose being higher is due to a false reading, either because of incidental residual carbohydrates on the hands, or deliberate, as has been noted in some anorexic patients, whereby they rub sugary sweets on their hands to avoid being picked up by the doctor.
Same patient, 20 year old female, BMI 17kg/m2, with some Lanugo hair noted. Finger prick glucose was 3.8mmol/L, and routine bloods were taken. Doctor rung by lab 1 hour later as plasma glucose was 2.6mmol/L.
What would the insulin and C-peptide result be if they had been measured?
(a) Low insulin, low C-Peptide
(b) Low insulin, high C-Peptide
(c) High insulin, low C-Peptide
(d) High insulin, high C-Peptide
The correct answer is (a) Low insulin, low C-Peptide.
1 day old neonate who is jittery and not feeding. Born by caesarean at 34 weeks gestation. Lab glucose 1.9mmol/L. Glucose improved on feeding, but low blood glucose 4 hours after feed. Beta-hydroxybutyrate measured at time of hypo and was negative.
What's absence of beta-hydroxybutyrate signify?
(a) Insulin deficiency
(c) Fatty acid oxidation defect
(d) Starvation and glycogen depletion
(e) Glucagon deficiency
The correct answer is (c) Fatty acid oxidation defect.
Beta-hydroxybutyrate is a ketone body. So free fatty acids would be high in this neonate as there is a defect preventing the conversion to ketones.
45 year old lady brought in fitting. Recurrently seen GP in previous months due to weight gain and increased appetite. Husband reports personality change in last few months.
Glucose 1.9 mmol/L, Insulin 35 mu/L and C-peptide 1000pmol/L.
What is the most likely diagnosis?
(a) Cushings syndrome
(b) Addison's disease
(c) Sulphonylurea excess
(e) Need more information
The correct answer is (e) Need more information.
Two things can result in this picture, either an insulinoma or sulphonylurea excess. A sulphonylurea screen needs to be done and if that's negative it would point towards an insulinoma.
9 year old boy brought in fitting. Glucose 1.9mmol/L, Insulin 205mu/L, C peptide <33pmol/L.
What is the most likely cause of the low blood glucose in this boy?
(a) Factitious insulin
(b) Epileptic fit
(c) Stress response to exercise
(e) Need more information
The correct answer is (a) factitious insulin.
Only exogenous insulin can produce a picture where there is high insulin and low C-peptide. They are produce in equimolar amounts by the body, so this has to be factitious insulin.
60 year old cachectic man found unconscious by his daughter. He's a smoker and his glucose was 1.9mmol/L. Hypoglycaemia persists so given a glucose infusion. Insulin and C-peptide are undetectable, free fatty acids are also undetectable and ketones are negative.
What diagnosis is most likely in this man?
(a) Benign insulinoma
(b) Non-islet cell tumour hypoglycaemia
(c) Malignant insulinoma
(d) Addison's disease
The correct answer is (b) Non-islet cell tumour hypoglycaemia.
In non-islet cell tumour hypoglycaemia there is a tumour that causes a paraneoplastic syndrome with secretion of 'big IGF-2'. Big IGF2 binds to IGF-1 receptor and insulin receptor. This is seen in mesenchymal tumours such as mesothelioma or fibroblastoma, as well as epithelial tumours such as carcinoma.
Levels of glucose, insulin, c-peptide, FFA and Ketones are all suppressed.
What is the pathological process in Gilberts Syndrome?
(a) Reduced activity of Aspartate transaminase
(b) Complete deficiency in UDP glucuronyl transferase
(c) Reduction in UDP glucuronyl transferase activity to 30%
(d) Slight obstruction in bile ducts of patients, causing a harmless increase in conjugated bilirubin.
(e) Mutation in albumin that causes bilirubin to be unable to bind to it, causing higher levels of unbound bilirubin in the blood.
The correct answer is (c) Reduction in UDP glucuronyl transferase activity to 30%.
The unconjugated bilirubin is tightly albumin bound and does not enter the urine.
(b) refers to what you'd find in Crigler-Najjar syndrome, an autosomal recessive disease that knocks out the enzyme.
All the rest are bollocks that I made up.
Which of the following is the most representative of acute liver function?
(a) Prothrombin time
(d) Alanine amino transferase
(e) Aspartate amino transferase
(f) Alkaline phosphatase
(g) Gamma glutamyl-transpeptidase
The correct answer is (a) Prothrombin.
If you fail to make clotting factors, the prothrombin time rapidly increases, making it an excellent marker for acute liver damage.
Albumin(b) is a good marker of chronic liver function, as the half life is a lot longer
Albumin, clotting factors and bilirubin (c) are all markers of liver function.
The other tests are enzymes which might indicate liver damage but are not truly tests of liver function.
Which of the following is caused by B1 deficiency?
(c) Pernicious anaemia
(f) Neural tube defects.
The correct answer is (d) Beri-Beri.
Rickets (a) is a deficiency in vitamin D.
Scurvy (b) is a deficiency in vitamin C.
Pernicious anaemia (c) is a deficiency in vitamin B12.
Pellagra is a deficiency in vitamin B3
Neural tube defects are caused by deficiency in folate, which is vitamin B9
45 year old man presents with jaundice to his GP. He denies excessive alcohol intake, though admits he does enjoy a glass of wine or two. He has no pain anywhere in his abdomen. He has experienced some weight loss over the past two months but reports no fevers. He has no family history of disease, and on abdominal examination he has a palpable gallbladder but no hepatomegaly.
What is the most likely cause for this man's jaundice?
(c) Carcinoma of the head of the pancreas
(e) Hepatocellular carcinoma
The correct answer is (c) Carcinoma of the head of the pancreas.
Following Courvoisier's law, in the presence of jaundice, if the gall bladder is palpable the cause is unlikely to be gall stones. Given the painless jaundice and palpable gallbladder against the background of weight loss and lack of fever this is most likely a carcinoma of the head of the pancreas causing an obstructive jaundice.
31 year old female seen in GP with general malaise and feeling unwell and "not herself" for about two weeks. She had had a few episodes of vomiting. Routine bloods showed an Hb of 12, an alkaline phosphatase of 165 (normal range 30-130) and a raised alpha feto protein. The GP immediately referred her to the hepatologists on a two week wait.
What is the most likely cause of this patient's symptoms?
(b) Hepatocellular carcinoma
(c) Metastatic liver cancer
(d) Autoimmune hepatitis
The correct answer is (e) pregnancy.
Pregnancy can create a host of symptoms that are non-specific and alarming, especially if it's not known the patient is pregnant. Vomiting is a normal part of first trimester pregnancy, Hb falls as part of normal pregnancy, alk phosphatase can double or triple by the third trimester and alpha feto protein, a marker of hepatocellular carcinoma, can be raised as part of normal pregnancy.
Pregnancy should always be considered a possibility in any woman of childbearing age.
A buildup of which part of the haem synthesis pathway causes neurovisceral symptoms of porphyria?
(b) 5-Aminolaevulinic acid
(d) Uroporphyrinogen III
(e) Protoporphyrin IX
The correct answer is (b) 5-Aminolaevulinic acid.
Skin lesions are caused by excess porphyrinogens which are oxidised to porphyrins then in the presence of UV light they become activated and cause the skin lesions.
22 year old female just returned from holiday where she'd been drinking heavily. She was complaining of abdominal pain, nausea and vomiting and had become increasingly paranoid. After returning to the UK she had some tonic/clonic seizures, and reported blurred vision and seeing flashing lights.
Serum Na 118 mmol/L, Urine ALA 207 (<3.8), urine PBG 215 (<1.5), hydroxymethylbilane synthase 11 (20-42).
What is the cause of this patient's symptoms?
(a) Acute intermittent porphyria
(b) Porphyria cutanea tarda
(c) Acute alcohol-induced hepatitis
(d) Illicit drug use
(e) Variegate porphyria
The correct answer is (a) acute intermittent porphyria.
AIP is caused by a deficiency in HMB synthase, which is why ALA and PBG are both raised as they are upstream of HMB synthase. This is not a complete deficiency, usuallly there is around 30-50% of normal function, but certain triggers overly tax the pathway and cause an attack, as detailed in the next question...
Which of the following is not a trigger of Acute intermittent porphyria?
(a) Excess carbohydrates
The correct answer is (a) Excess carbohydrates.
In fact, good diet and carbohydrate intake is recommended to prevent attacks of AIP, as carbohydrate levels inhibit the action of ALA synthase. IV carbohydrate is useful in the management of an acute episode of AIP, and reduced calorie intake can be a trigger of AIP.
During acute porphyria, the most useful sample to send is?
(e) Skin Biopsy
The correct answer is (c) urine.
Which of the following hormones is not low in pituitary failure?
The correct answer is (c) Aldosterone.
Pituitary failure does not equal adrenal failure, Aldosterone production and release is controlled by the renin-angiotensin system which is unaffected by pituitary failure.