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Pathology Amber > Chemical pathology > Flashcards

Chemical pathology Flashcards

1
Q

How do you calculate osmolarity?

A

Osmolarity = charged ions + uncharged ions
= 2(cations) + Urea + Glucose mosmol/kg

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2
Q

How do you calculate anion gap?

A

Anion gap = cations - known anions (need HCO3- and Cl-)

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3
Q

What is the acid base equilibrium equation?

A

H+ + HCO3- = CO2 + H20

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4
Q

What acid-base disturbance is characterised by a low pH and a high PCO2?

A

Respiratory acidosis

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5
Q

What acid-base disturbance is characterised by a low pH and a low pCO2?

A

Metabolic acidosis

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6
Q

What acid-base disturbance is characterised by a high pH and a low pCO2?

A

Respiratory alkalosis

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7
Q

What acid-base disturbance is characterised by a high pH and a high pCO2?

A

Metabolic alkalosis

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8
Q

What acid-base disturbance is characterised by a high pH and a high pCO2?

A

Metabolic alkalosis

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9
Q

What metabolic bone disease would give you all normal parameters except raised ALP?

A

Paget’s disease

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10
Q

What are the primary defects in OP, OM/rickets, Paget’s bone disease and Renal bone disease?

A

OP: bone loss
OM: low vit D
Paget’s: Remodelling
PTH bone disease: high PTH
Renal bone disease: low 1a-hydroxylation, aluminium toxicity?

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11
Q

What is the commonest biological cause of primary hyperparathyroidism?

A

Parathyroid tumour/adenoma

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12
Q

What is the aetiology of familial hypocalciuric hypercalcaemia (FHH/FBH)?

A

A CaSR inactivating mutation which makes it less sensitive to high serum Ca2+ levels. The receptor therefor has a higher set point for PTH release causing permanent mild hypercalcaemia.

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13
Q

Define AKI

A

A rapid reduction in kidney function. This leads to an inability to maintain electrolyte, acid-base and fluid homeostasis.

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14
Q

What is AKI management?

A

Medical emergency
Refer to nephrologist for Dx and Tx

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15
Q

How is AKI classified?

A

3 stages of AKI

1) increase in creatinine of 1.5-1.9x reference range / >=26umol/L
2) increase in creatinine of 2-2.9x reference range
3) increase in creatinine of >3x reference range

Urine output should also be <0.5ml/kg/hr for 6 hrs

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16
Q

What are the hallmarks of each type of AKI?

A

Pre-renal - reduced renal perfusion
Post-renal - physical obstruction to urine flow
Intrinsic/renal - damage to any part of nephron

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17
Q

What are the 5 stages of CKD?

A

1) Kidney damage with normal GFR
2) Mild decrease in GFR
3) Moderate decrease in GFR
4) Severe decrease in GFR
5) End-stage kidney failure

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18
Q

What are the consequences of CKD?

A

1) Failure of homeostatic function -> hyperkalaemia, acidosis
2) Progressive failure of hormonal function -> decreased EPO, vit D, RAAS
3) CVD -> vascular calcification, uraemic myopathy (3 phases)

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19
Q

What is the normal range for bilirubin?

A

5-17

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20
Q

What is the condition characterised by all normal liver function tests except a high bilirubin level of 45 (5-17 normal range)?

A

Gilbert’s syndrome

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21
Q

A patient comes in and is jaundiced and complaining of a dull pain in their right epigastric region. Their stools have been a weird pale yellow colour since 2 days ago. You test their urine for the presence of urobilinogen and it is negative, what is the diagnosis?

A

Obstructive jaundice - blockage of the biliary tree

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22
Q

Which of these is the most representative of liver function?

a) Prothrombin time
b) Albumin
c) Bilirubin
d) Alanine amino transferase
e) Aspartate amino transferase
f) Alkaline phosphatase
g) Gamma GT

A

a) Prothrombin time
Clotting is the best indicator of hepatic function.

Albumin and bilirubin are okay

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23
Q

What is the normal range for prothrombin time?

A

12-14 seconds

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24
Q

What are the ddx for a hyperbilirubinaemia of 90?

A

Pre-hepatic: Gilbert’s syndrome, haemolytic anaemia
Hepatic: Viral hepatitis, alcoholic hepatitis, cirrhosis
Post-hepatic: Gallstones, pancreatic cancer

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25
Q

What do raised levels of AST, ALT and ALP mean respectively?

A

AST - hepatocyte damage (NR <50)
ALT - hepatocyte damage (NR <50)
ALP - Obstructive jaundice (NR <130)

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26
Q

In a patient with ALP of 200, ALT 1500 and AST 750, what is the likely pathology?

a) Pre-hepatic
b) Post-hepatic
c) Hepatic

A

c) Hepatic

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27
Q

What is a side effect of pabrinex?

A

Dark yellow urine

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28
Q

Which of these is causes by thiamine deficiency (B1)?
Rickets
Scurvy
Beri Beri
Pellagra
Pernicious anaemia
Neural tube defects

A

Beri beri

Rickets - vitamin D
Scurvy - vitamin C
Pellagra - Niacin deficiency (B3)
Pernicious anaemia - B12 (IF deficiency)
Neural tube - folate deficiency

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29
Q

On examination, a patient has multiple spider naevi, palmar erythema, dupuytren’s contracture and gynaecomastia, which one of the following is most likely?
Chronic stable liver disease
Portal hypertension
Jaundice
Hepatitis
Liver failure
Obstruction of bile ducts

A

Chronic stable liver disease

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30
Q

What is this and what does it signify?

A

A visible vein on the anterior abdominal wall/Caput medusae
Portal hypertension/increase in umbilical venous pressure

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31
Q

Given portal hypertension, what other feature are you most likely to see?

a) hepatomeglay
b) splenomegaly
c) palpable bladder
d) bilateral, palpable kidneys
e) enlarged prostate gland on PR

A

b) splenomegaly - presuure in the portal vein increases -> pressure in the splenic vein increases -> pressure in the spleen increases and it enlarges -> splenomegaly

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32
Q

A patient has visible veins on his anterior abdomen, shifting dullness and splenomegaly on examination. What is the diagnosis?

Chronic liver disease

Jaundice

Hepatitis

Liver failure

Portal hypertension

Obstruction of bile ducts

A

Portal hypertension

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33
Q

What does a tremorous flap of the hands suggest when asked to keep hands 90 degrees from extended arms (similar hypercapnic flap)?

A

Liver failure - may be due to ammonia (unknown)

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34
Q

What are the hallmarks of liver failure?

A

Failure of: synthetic functions, clotting factor, albumin, bilirubin clearance, ammonia clearance (hepatic encephalopathy)

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35
Q

What are the sites of porto-systemic anastamoses?

A

Sites where portal circulation meets systemic circulation

Oesophagus

Abdominal wall near umbilicus

Rectum

Near spleen

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36
Q

What do scratch marks on the skin with jaundice suggest?

A

Obstruction of the bile ducts - gall stones or pancreatic carcinoma (head of the pancreas)

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37
Q

What is Couarvoisier’s law?

A

If a patient is jaundiced and their gallbladder is palpable it is likely to be pancreatic cancer rather than gallstones as gallstones cause the gallbladder to shrink and become fibrotic.

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38
Q

What do stellate cells activate into when there is liver damage?

A

When there is liver damage, quiescent stellate cells within the space of disse become activated and differentiate into myelofibroblasts which produce collagen which deposits fibrous scar tissue within the liver.

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39
Q

What happens to the cells of the liver when the liver is damaged ?

A

Hepatocytes lose their microvilli

Stellate cells differentiate into myelofibroplasts

Endothelial cells become continous and joined together - loss of fenestrations

Kupffer cells also become activated

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40
Q

What is micronodular cirrhosis most associated with?

A

Alcohol abuse, alcoholic liver disease

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41
Q

What is macronodular cirrhosis most associated with?

A

Viral hepatitis

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42
Q

What are the complications of liver cirrhosis?

A

1) Portal hypertension
2) Hepatic encephalopathy
3) Liver cell cancer

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43
Q

What does this picture show?

A

Spotty necrosis in acute hepatitis

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44
Q

What is the difference between the left and right picture?

A

Left picture: normal

Right picture: increasing fibrosis - not just in portal triad/tract but towards central vein etc. This causes intrahepatic shunting, as blood cannot enter the hepatocytes.

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45
Q

What does this picture show?

A

Fatty liver

Hepatocytes containing fat

Alcoholic liver disease

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46
Q

What does this picture show?

A

Alcoholic hepatitis - ballooning of cells (collapsed cytoplasm), mallory denk bodies, pericellular fibrosis, fat

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47
Q

What does this picture show?

A

Granulomatous disease centred around a hepatic bile duct that is being destroyed and is chronically inflamed.

Primary biliary cholangitis.

This can progress to a cirrhosis of the bile duct if not trated.

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48
Q

What does this picture show?

A

Pink globules show accumuations of alpha 1 anti trypsin within hepatocytes.

Alpha-1 antitrypsin deficiency in the liver.

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49
Q

What does this picture show?

A

Liver cell adenoma

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50
Q

What does this picture show?

A

Intrahepatic cholangiocarcinoma

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51
Q

Which of these is the commonest liver carcinoma?

a) Liver cell carcinoma
b) Cholangiocarcinoma
c) Metastatic adenocarcinoma

A

c) Metastatic adenocarcinoma

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52
Q

Which of these is not associated with fatty change in the liver?

a) Hepatitis B
b) Hepatitis C
c) Alcohol
d) Diabetes

A

Hepatitis B and Hepatitis C are not associated with fatty change in the liver.

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53
Q

Which of these is not associated with genetic haemochromatosis?

a) Kaiser Fleischer rings
b) Diabetes
c) Myocardial damage
d) Cirrhosis

A

a) Kaiser Fleischer rings

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54
Q

A 76 year old patient with a previuos MI has a BP of 140/80 on atenolol.

His LDL is 3.0mmol on atorvostatin 80mg.

Is there evidence to lower his BP further?

A

Yes, the patient should be offered thiazide diuretics or calcium channel blockers as intensive treatment will lower the risk of further cardiovascular disease, CV death, MI, acute coronary syndrome or heart failure.

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55
Q

Explain absolute reduction

A

An absolute reduction of 2% with regards to an outcome means that if the intervention is followed by 100 people, 2 less people will encounter the outcome as opposed to a group of 100 people with no intervention.

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56
Q

What are some treatments for lipid and cholesterol control is a patient is statin intolerant?

A

Ezetemibe

Plasma exchange

Evolocumab (PCSK9 monoclonal Ab)

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57
Q

What is PCSK9?

A

Proprotein convertase subtilisin kexin 9 (PCSK9)

PCSK9 regulates levels of the LDL receptor. It forms a complex with LDL R, which is endocytosed and then digested by lysosomal enzymes.

Gain-of-function mutations in PCSK9 reduce LDL receptor levels in the liver, resulting in high levels of LDL cholesterol in the plasma.

Loss-of function mutations in PCSK9 increase LDL receptor levels in the liver, resulting in lower LDL cholesterol levels and conferring protection from coronary heart disease.

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58
Q

What is an example of a monoclonal Ab for PCSK9?

A

Evolocumab

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59
Q

What is the effect on number needed to treat, if your risk reduction is extremely small?

A

High number needed to treat

Likely to have little/no effect on mortality

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60
Q

What condition is PCSK9 inhibitors approved for?

A

Familial Hypercholesterolaemia

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61
Q

How many years does good glucose control take to make a difference to a patient’s health (UK prospective diabetes study i.e. newly diagnosed diabetes patients)?

A

It takes a long time i.e. 12-15 years after diagnosis, to make a real difference in terms of outcomes.

After a patient stops intensive glucose control, they have 10 years of long-term health benefits compared to lax glucose control. This is called the legacy effect.

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62
Q

What are the landmark studies done into blood glucose control?

A

DCCT - T1DM - good control = improved outcomes

UKPDS - intensive control improves outcomes after around 15 years, 10 years worth of legacy effects - long-term benefits to health after intensive control ceases

ACCORD - Old people with coronary artery disease + intensive control = death

ADVANCE - Not much difference between intensive and conventional control in diabetes vascular patients - perhaps a reduction

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63
Q

What was presumed the culprit drug of the ACCORD study?

A

Rosaglitazone - now banned as increases mortality

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64
Q

What is an SGL2 inhibitor example?

A

Empagliflozin, used for diabetes

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65
Q

What effects do SGL2 inhibitors have?

A

HbA1c reduction, weight loss, systolic BP reduction, Waist circumference reduction, early reduction in diastolic BP, treatment of heart failure, protect the kidneys (sustain eGFR)

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66
Q

Which study on glucose control suggested that tight control increases mortality?

a) ACCORD
b) ADVANCE
c) DCCT
d) UKPDS
e) No study

A

a) ACCORD

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67
Q

What does SGLT2 and GLP-1 stand for?

A

XXXX

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68
Q

What is the inheritance pattern of familial hypercholesterolaemia?

A

Autosomal dominant

Rare types can be inherited via an autosomally recessive pattern

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69
Q

What is the most common electrolyte abnormality in hospitalised patients?

A

Hyponatraemia

A serum sodium level of less than 135 mmol/L

1/4 patients have hyponatraemia

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70
Q

What is the underlying pathogenesis of hyponatraemia?

A

Increased extracellular water - ‘dilution’

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71
Q

Which hormone controls water balance?

A

Anti-diuretic hormone (vasopressin)

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72
Q

How does anti-diuretic hormone/vasopressin work?

A

Acts on V2 receptors in the collecting duct, upregulates insertion of aquaporin-2 in the collecting duct wall which leads to more water reabsorption into the blood.

Also acts on V1 receptors in vascular smooth mucle, causing vasoconstriction typically at higher concentrations.

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73
Q

What are the 2 main stimuli for ADH secretion?

A

1) Increased serum osmolality - this is mediated by hypothalamic osmoreceptors
2) Low blood volume/pressure - this is mediated by baroreceptors in the carotids, atria and aorta

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74
Q

What makes you feel thirsty?

A

An increase in osmolality detected by the hypothalamic osmoreceptors

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75
Q

What is the first step in the clinical assessment of a patient with hyponatraemia?

A

Clinical assessment of volume status

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76
Q

When vomiting, why do we become hyponatraemic?

A

Because we lose blood volume when we vomit through loss of fluid. This is detected by the baroreceptors at the carotids, atria and aorta. This leads to increased water retention as more ADH is secreted by the posterior pituitary. This leads to increased extracellular water compared to sodium concentration.

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77
Q

What is the most reliable indicactor of hypovolaemia?

A

Low urine Na+

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78
Q

What are the causes of a hyponatraemic hypovolaemia?

A

Diarrhoea

Vomiting

Diuretics

Salt losing nephropathy

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79
Q

What are the causes of a hyponatraemic euvolaemia?

A

Hypothyroidism

Adrenal insufficiency

SIADH

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80
Q

What are the causes of hyponatraemia in a hypervolaemic patient?

A

Cardiac failure

Cirrhosis

Nephrotic syndrome

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81
Q

Why do you get a low urine Na+ in hyponatraemic hypervolaemia?

A

Cardiac failure leads to a secondary hyperaldosteronism which leads to reabsorption of Na+. This means less Na+ is excreted in the urine.

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82
Q

How would you manage a hypovolaemic patient with hyponatraemia?

A

Volume replacement with 0.9% saline

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83
Q

How would you manage a hypervolaemic or euvolaemic patient with hyponatraemia?

A

Fluid restriction and treat the underlying cause

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84
Q

What does fluid restriction mean practically?

A

0.5-1L in 24 hours

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85
Q
A
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86
Q

What is the most important point to remember when correcting hyponatraemia?

A

Serum Na must not be corrected >8-10mmol/L in the first 24 hours. Risk of osmotic demyelination increases (central pontine myelionlysis) due to rapid shift in fluids within brain cells. This is a disruption of the blood brain barrier. Signs of central pontine myelionlysis include quadriplegia, dysarthria, dysphagia, seizures, coma and death.

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87
Q

What are the causes of hypernatraemia?

A

1) Unexplained water loss (GI loss, renal loss, sweat loss)
2) Patient cannot control water intake i.e. Alzheimer’s, baby, child

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88
Q

What investigations would you order in a patient with suspected diabetes insipidus?

A

Serum glucose (exclude diabetes mellitus)

Serum potassium (exclude hypokalaemia - exclude nephrogenic DI)

Serum calcium (exclude hypercalcaemia - causes resistance to ADH, nephrogenic DI)

Plasma and urine osmolality

Water deprivation test

Serum sodium

89
Q

How do we treat hypernatraemia?

A
  • Dextrose 5%
  • May need 0.9% saline for hypovolaemia
  • Serial 4/6 hrly serum Na+ measurements
90
Q

What are the effects of diabetes mellitus on serum sodium?

A

1) Hyperglycaemia draws water out of cells, leading to hyponatraemia
2) Osmotic diuresis in uncontrolled diabetes, leads to loss of water and hypernatraemia

91
Q

What hormones are involved in renal regulation of potassium?

A

Angiotensin 2

Aldosterone

92
Q

What are the 2 stimuli for normal aldosterone production?

A

Angiotensin 2

High levels of K+

93
Q

How does aldosterone lead to more K+ excretion?

A

1) Aldosterone binds to intracellular principal cell mineralocorticoid receptor
2) This leads to less degradation of epithelial sodium channels in the luminal wall (via expression of SGK1 and inhibition of Nedd4-2)
3) This increases the number of open sodium channels in the luminal wall
4) This leads to increased reabsorption of Na+ from lumen
5) This leads to the lumen becoming more electronegative and a electrical gradient is created
6) Potassium then moves down this electrical gradient
7) More potassium is secreted into the lumen and excreted into the urine

94
Q

What are the causes of hyperkalaemia?

A

1) Renal impairment (reduced renal excretion) - Reduced GFR - renal failure, CKD
2) Drugs: ACE inhibitors, Angiotensin 2 receptor blockers, spironolactone
3) Low aldosterone - Addison’s disease, T4 renal tubular acidosis (low renin, low aldosterone)
4) Release from cells: Rhabdomyolysis, acidosis

95
Q

What is the main ECG change associated with hyperkalaemia?

A

Peaked T waves

96
Q

How would you manage a patient with hyperkalaemia?

A

1) 10ml 10% calcium gluconate

2) 50 ml (50%/10 or 20% usually!) dextrose with 10 units insulin

3) Nebulised salbutamol
4) Tx underlying causes

*Treat when potassium is >6-6.5mmol/L or ECG changes*

97
Q

What are the causes of hypokalaemia?

A

1) GI loss - diarrhoea and vomiting
2) Renal loss - loop diuretics, hyperaldosteronism etc
3) Redistribution into cells - via insulin, beta agonists etc
4) Rare causes - renal tubular acidosis T1 and 2, hypomagnesaemia

98
Q

What are the clinical features of hypokalaemia?

A

Polyuria

Polydipsia (nephrogenic DI)

Muscle weakness

Cardiac arrhythmias

99
Q

What screening test would you order in a patient with hypokalaemia and hypertension?

A

Aldosteron:Renin ratio

(High aldosterone: Low Renin) -> high ratio

100
Q

How would you manage a patient with hypokalaemia?

A

Serum potassium 3-3.5mmol/L: Oral potassium chloride (2 SandoK tablets tds for 48 hrs)

Recheck serum potassium

Serum potassium <3mmol/L: IV potassium chloride (maximum rate 10mmol/hr, rates >20mmol/hr are highly irritating to peripheral veins)

Tx underlying cause i.e. surgery (adrenal adenoma causing conn’s), spironolactone etc

101
Q

Hypokalaemia is a side effect of which of the following drugs?

a) Furosemide
b) Bendroflumethiazide
c) Salbutamol
d) Ramipril

A

a) Furosemide - loop diuretic - leads to more Na+ being delivered to the distal tubules of the nephrons, leading to more Na+ reabsorption and K+ excretion
b) Bendroflumethiazide - thiazide diuretic - leads to more Na+ being delivered to the distal tubules of the nephrons, leading to more Na+ reabsorption and K+ excretion

102
Q

Hyperkalaemia is a side effect of which of the following drugs?

a) Furosemide
b) Bendroflumethiazide
c) Salbutamol
d) Ramipril

A

d) Ramipril

Ramipril is an ACE inhibitor and disrupts the Renin-Angiotensin-Aldosterone axis by preventing the Angiotensin Converting Enzyme within the lung from converting Angiotensin 1 to Angiotensin 2. This results in a lack of adrenal stimulation to release aldosterone, which then leads to more Na+ being excreted and more K+ being absorbed.

103
Q

A 67 year old man was started on bendroflumethiazide for hypertension 2 weeks ago. He has D and V for 2 days. He has dry mucous membranes and decreased skin turgor.

U&Es:

Na+ 129 mmol/L

K+ 3.5 mmol/L

Ur 8.0 mmol/L

Cr 100 Umol/L

What is the diagnosis?

A

Hypovolaemic hyponatraemia

Causes by GI loss - D&V

Mx: 0.9% saline volume replacement

104
Q

57 year old woman is breathless on lying flat. Her PMH includes a non-stemi. She is on ramipril, bisoprolol, aspirin and simvastatin. She has elevated JVP, bibasal crackles and bilateral leg oedema.

U&Es:

Na+ 128 mmol/L

K+ 4.5 mmol/L

Ur 8.0 mmol/L

Cr 100 umol/L

What is the diagnosis?

A

Hypervolaemia hyponatraemia

Mx: Fluid restriction 0.5-1 L (24hrs)

Tx underlying cause: Heart failure

105
Q

A 55 year old man has jaundice. He has a past Hx of excessive alcohol intake. He has multiple spider naevi, shifting dullness and splenomegaly.

U&Es:

Na+ 122mmol/L

K+ 3.5 mmol/L

Ur 2.0 mmol/L

Cr 80 umol/L

What is the diagnosis?

A

Hypervolaemic hyponatraemia due to liver cirrhosis

Mx: Fluid restriction 0.5-1 L (24 hrs)

Tx underlying cause -> liver transplant? Stop drinking?

106
Q

How does liver cirrhosis lead to hyponatraemia?

A

In cirrhosis we have excess nitrous oxide NO production

This causes vasodilation

This reduces blood pressure

Baroreceptors detect this

In turn we secrete more ADH

This leads to more water retention

This causes hyponatraemia

107
Q

A 40 year old woman presents with fatigue, weight gain, dry skin and cold intolerance. On examination she looks pale.

U&Es:

Na+ 130mmol/L

K+ 4.2 mmol/L

Ur 5 mmol/L

Cr 65 umol/L

What is the diagnosis?

A

Euvolaemic hyponatraemia due to hypothyroidism

Ix: TFTs

Mx: Fluid restriction

Tx underlying cause: Levothyroxine (thyroxine replacement)

108
Q

A 45 year old woman presents with dizziness and nausea. On examination, she looks tanned and has postural hypotension.

U&Es:

Na+ 128 mmol/L

K+ 5.5 mmol/L

Ur 9 mmol/L

Cr 110 umol/L

A

Addison’s disease

+

Adrenal insufficiency

Ix: Short synacthen test

Mx: Hydrocortisone (GC) and Fludrocortisone (MC)

109
Q

A 62 yr old man has chest pain, cough and weight loss. He looks cachectic. He has a 30 pack year smoking history.

U&Es:

Na+ 125 mmol/L

K+ 3.5 mmol/L

Ur 7 mmol/L

Cr 85 umol/L

What is the diagnosis?

A

SIADH - due to underlying lung cancer

Ix: Brain CT, CXR, assess volume status, TFTs, Adrenal function, plasma (decreased) and urine osmolality (increased)

Mx: Fluid restriction, demeclocycline (monitor U&Es), tolvaptan, Tx underlying cause - surgery or

110
Q

A 20 year old man presents with polyuria and polydipsia. On examination, he has a bitemporal hemianopia.

U&Es:

Na+ 150 mmol/L

K+ 4.0 mmol/L

Ur 5 mmol/L

Cr 70 umol/L

What is the diagnosis?

A

Central diabetes insipidus

(unreplaced water loss, causing hypernatraemia)

111
Q

A 65-year-old man with T2DM and HTN presents with malaise and drowsiness. He is on a basal bolus insulin regimen, ramipril, amlodipine, simvastatin and aspirin.

U&Es:

Na+ 125 mmol/L

K+ 6.5 mmol/L

Ur 18 mmol/L

Cr 250 umol/L

What is the diagnosis?

A

Reduced GFR (renal impairment) and ACE inhibitor causing hyperkalaemia

Ix: Do ECG -> peaked T waves should be present, blood glucose levels

Mx: 10ml 10% calcium gluconate

200/100ml 10/20% dextrose + 10 units of insulin

Nebulised salbutamol

Tx underlying cause

112
Q

A 50 year old man is referred with hypertension that has been difficult to control despite maximum doses of amlodipine, ramipril and bisoprolol.

U&Es:

Na+ 140 mmol/L

K+ 3 mmol/L

Ur 4 mmol/L

Cr 70 umol/L

What is the diagnosis?

A

Hypokalaemia due to Conn’s syndrome

Ix: Aldosterone:renin ratio (high in Conn’s)

Mx: Oral potassium chloride 2 tablets of SandoK tablets tds for 48 hrs

Recheck U&Es

113
Q

When might you see a result of hyperkalaemia and hypernatraemia?

A

Diabetic ketoacidosis

114
Q

Piuitary failure causes hypotension

True

OR

False

A

False - the body still creates aldosterone

115
Q

What are the 6 hormones released from the anterior pituitary?

A
  • Growth hormone
  • Prolactin
  • LH and FSH
  • ACTH
  • TSH
116
Q

What are the hypothalamic hormones that act on the anterior pituitary?

A
  • Growth Hormone Releasing Hormone
  • Dopamine (-ve stimulation for prolactin release)
  • Luteinising Hormone Releasing Hormone
  • Thyroid Releasing Hormone
  • Corticotrophin Releasing Hormone
117
Q

What complication of a large pituitary tumour should you look out for?

A

Bitemporal hemianopia

118
Q

A 30 year old female comes in with galactorrhoea. A 2cm pituitary macroadenoma is found on a CT scan and her prolactin level comes back at 30,000 (normal < 600). She has not had sexual intercourse.

What is the diagnosis?

A

Prolactinoma

119
Q

What investigation should be completed, given the diagnosis of prolactinoma?

A

Combined pituitary function tests

LH, FSH, TFTs, GH/IGF1, ACTH, Cortisol

To ensure that the pituitary gland responds adequately to a metabolic stress (ACTH + GH)

We would therefore administer LHRH and TRH and a stressor too

120
Q

To complete a combined pituitary function test, what stress should be applied?

A

Hypoglycaemia - make the patient around 2mmol/L blood glucose

This will increase CRH and thus ACTH thus Cortisol

Additionally, this will increase GHRH and thus GH

121
Q

Out of all the pituitary replacement hormones, which is urgent?

A

Hydrocortisone

122
Q

What is the order of given tx for a patient with prolactinoma and hypopituitarism?

A

1) Hydrocortisone
2) Thyroxine
3) Oestrogen
4) GH if deficient, short and young
5) Tx prolactinoma (dopamine agonist): bromocriptine or cabergoline (need psychiatry input - as can cause psychosis)

123
Q

In a patient who is 27, who also has a vision field defect and a prolactin level of 2944, a combined pituitary function test is completed and there is no difference to any hormone levels, what is the diagnosis?

A

Non-functioning pituitary adenoma

124
Q

Which treatment is not needed for a prolactinoma?

a) Fludricortisone
b) Hydrocortisone
c) Thyroxine
d) Oestrogen
e) GH

A

a) Fludrocortisone replacement

125
Q

What treatment is required alongide hormone replacement therapy in a 27 year old patient?

a) Carbimazole
b) Dexamethasone
c) Cabergoline
d) Octreotide
e) None

A

e) None - no drug treatment required - pt may have surgery soon, patient could be given cabergoline to bring down the prolactin (good for woman wanting normal periods and pregnancy), octreotide could also be used

126
Q

A 28 year old has a visual field defect and is put forward for combined pituitary function testing. Her growth hormone before the test is 30mmol/L and increases to 60.2mmol/L during the test. The prolactin was also consistently >600mmol/L, rising slightly during the test.

All other hormones were produced at low levels and did not change during the test. What is the diagnosis?

A

Acromegaly

127
Q

In a patient with suspected Acromegaly, what dynamic test is needed for the diagnosis?

a) Low dose dexamethasone suppression test
b) High dose dexamethasone suppression test
c) Synacthen test
d) Glucose tolerance test
e) TRH stimulation test

A

d) Glucose tolerance test

128
Q

Name one other test apart from glucose tolerance test to confirm the diagnosis of Acromegaly?

A

Serum IGF-1

129
Q

What is the best tx for acromegaly?

a) Pituitary surgery
b) Pituitary radiotherapy
c) Cabergoline
d) Octreotide
e) All of the above

A

1) Pituitary surgery
2) Pituitary radiotherapy
3) Cabergoline
4) Octreotide

130
Q

What causes the adrenal glands to change size?

A

Shrink - Adrenal atrophy - Addison’s disease or long-term corticosteroid therapy

Grow - bilateral cortical hyperplasia - pituitary adenoma secreting ACTH (Cushing’s disease), or Cushing’s syndrome from ectopic ACTH production, or idiopathic adrenal hyperplasia.

131
Q

The zona fasciculata produces cortisol - true or false?

A

True

132
Q

A patient has some TFTs done and the results are as follows:

Free T4: <5nM

TSH: >50 U/L

What is the diagnosis?

A

Primary hypoparathyroidism

133
Q

U&Es are ran in a patient and the results are as follows:

Na+ 125

K+ 6.5

Glucose 2.9 mM

What is the likely pathology?

A

These results show hyponatraemia, hyperkalaemia and hypoglycaemia. Therefore pointing towards both a mineralocorticoid and glucocorticoid deficiency within the patient. This would be consistent with Addison’s disease.

134
Q

What is the diagnosis in patients with Addison’s disease and primary hypothyroidism?

A

Polyglandular autoimmune syndrome type 2

Historically known as: Schmidt’s syndrome

(Auto-immune diseases commonly occur together)

135
Q

What dynamic test investigation will confirm a diagnosis of Addison’s disease?

a) Low dose dexamethasone suppression test
b) High dose dexamethasone suppression test
c) Synacthen test
d) Glucose tolerance test
e) TRH stimulation test

A

c) Synacthen test (short)

136
Q

How is the synacthen test for Addison’s disease carried out?

A

A blood test is taken from a vein in your arm to measure cortisol and ACTH. You will be given an injection of synacthen (tetracosactide), which stimulates the adrenal glands to produce Cortisol. You will wait in the waiting room for 30 minutes. A final blood test will be taken for cortisol, this completes the test (short synacthen test). If the cortisol does not go up then they have Addison’s.

i.e. confirmatory results:

ACTH >100 ng/dl

Cortisol <10nM

NOTE: Long synacthen test: a blood sample is taken at the start of the test, an injection of tetracosactide is given and blood samples are taken at regular intervals over a 24-hour period.

137
Q

What is the low-dose dexamethasone suppression test used to diagnose?

A

Cushing’s syndrome

138
Q

Define phaeochromocytoma

A

Adrenal medullary tumour secreting adrenaline

139
Q

What is the difference between Cushing’s disease and Cushing’s syndrome?

A

Cushing’s disease is a type of Cushing’s syndrome. Cushing’s disease is caused by a benign tumor located in the pituitary gland that secretes too much ACTH (adrenocorticotropic hormone), which in turn increases cortisol.

140
Q

What treatment is given urgently in patient’s with phaeochromocytoma?

A

Alpha blockers

141
Q

Define Conn’s syndrome

A

The adrenal gland secretes a high level of aldosterone autonomously. This causes hypertension, which in turn suppresses renin at the juxto-glomerular-apparatus.

142
Q

A 34 year old woman presents to hospital with T2DM, hypertension and bruising. Her U&Es are as follows:

Na+ 146

K+ 2.9

U 4.0

Glucose 14.0

Aldosterone <75

Renin low

True or False:

This excludes Conn’s and suggests another hormone is causing the hypertension.

A

True

143
Q

If a patient’s cortisol level is 650nM on monday at 9am and then is <50nM on Wednesday after completing the low dose dexamethasone suppression test, what is the diagnosis?

A

This result shows successful cortisol suppression. Therefore the patient does not have Cushing’s syndrome.

144
Q

If a patient’s cortisol level is 650nM on monday at 9am and then is 500nM on Wednesday after completing the low dose dexamethasone suppression test, what is the diagnosis?

A

Cushing’s syndrome of indeterminate cause

145
Q

With a Cushing’s syndrome picture, what must we do next to investigate the pt?

A
  • Find out if she is on any steroids
  • Most likely to be pituitary dependent Cushing’s disease ->

Ix: Pituitary sampling

146
Q

If a high-dose dexamethasone suppression test is carried out and cortisol levels are successfully suppressed, following a weak result with low dose dexamethasone suppression test, what is the diagnosis?

A

Pituitary dependent Cushing’s disease

147
Q

What test has replaced high dose dexamethasone suppression test for investigating Cushing’s syndrome?

A

Pituitary sampling

(high dose suppression test masks other problems such as ectopic ACTH)

148
Q
A
149
Q
A
150
Q

Define compensation within Acid-Base handling

A

Compensation is the return of pH towards the normal range at the expense of other values

151
Q

What is the normal range for pH?

A

7.35-7.45

152
Q

What is a buffer?

A

A weak acid and its base

153
Q

What is a buffer commonly found in the renal tubular fluid and what is it’s buffering reaction?

A

Phosphate

H+ + HPO4- H2PO4

154
Q

What is the main buffer in the body?

A

Bicarbonate

155
Q

Where is bicarbonate regenerated?

A

The kidney

156
Q

In red blood cells what is the main buffer?

A

Haemoglobin. This reacts with H+ ions to form HHb.

157
Q

What is the interrelationship in Acid-Base balance?

A

Interrelationship between H+ ions being excreted by the kidney and CO2 being excreted by the lungs.

158
Q

What is the calculation for specificity?

A

TN/Everyone without the disease (TN+FP) *100%

159
Q

What is the formula for sensitivity?

A

TP/Everyone with the disease (TP+FN) * 100%

160
Q

What is the formula for positive predictive value?

A

TP/(TP+FP)

161
Q

What is the formula for negative predictive value?

A

TN/(TN+FN) * 100%

162
Q

What does a vitamin K (phytomeniadone) deficiency result in?

A

Defective clotting

163
Q

What does a vitamin E (Tocopherol) deficiency result in?

A

Anaemia/neuropathy/malignancy/ ischaemic heart disease

164
Q

What does a vitamin D (cholecalciferol) deficiency result in?

A

Rickets (children)

Osteomalacia (adults)

165
Q

What does a vitamin A (retinol) deficiency result in?

A

Colour blindness

166
Q

What is pellagra a deficiency to?

A

Vitamin B3 (niacin)

167
Q

What are the fat soluble vitamins?

A

A, D, E, K

168
Q

For each Clinical scenario below, choose the SINGLE most likely

A. To predict risk of myocardial infarction and decide of possible benefit of HMG-CoA reductase inhibition (statin therapy)

  1. Measurement of body mass index and waist circumference
  2. Measurement of serum leptin concentration
  3. Measurement of resting energy expenditure
  4. Measurement serum polyunsaturated fat concentration
  5. Measurement of total plasma cholesterol and/or low density lipoprotein cholesterol concentration
  6. Oral ferrous sulphate
  7. Oral Folic acid
  8. Oral vitamin K
  9. Parenteral thiamine (Pabrinex)
  10. Reducing saturated fat and increasing mono or polyunsaturated fat in diet
A

5.Measurement of total plasma cholesterol and/or low density lipoprotein cholesterol concentration

169
Q

For each Clinical scenario below, choose the SINGLE most likely

B. To assess the degree of obesity and resultant cardiovascular risk

  1. Measurement of body mass index and waist circumference
  2. Measurement of serum leptin concentration
  3. Measurement of resting energy expenditure
  4. Measurement serum polyunsaturated fat concentration
  5. Measurement of total plasma cholesterol and/or low density lipoprotein cholesterol concentration
  6. Oral ferrous sulphate
  7. Oral Folic acid
  8. Oral vitamin K
  9. Parenteral thiamine (Pabrinex)
  10. Reducing saturated fat and increasing mono or polyunsaturated fat in diet
A

1.Measurement of body mass index and waist circumference

170
Q

For each Clinical scenario below, choose the SINGLE most likely

C.To reduce risk of Wernicke’s encephalopathy in alcoholic patient admitted to hospital

  1. Measurement of body mass index and waist circumference
  2. Measurement of serum leptin concentration
  3. Measurement of resting energy expenditure
  4. Measurement serum polyunsaturated fat concentration
  5. Measurement of total plasma cholesterol and/or low density lipoprotein cholesterol concentration
  6. Oral ferrous sulphate
  7. Oral Folic acid
  8. Oral vitamin K
  9. Parenteral thiamine (Pabrinex)
  10. Reducing saturated fat and increasing mono or polyunsaturated fat in diet
A

9.Parenteral thiamine (Pabrinex)

171
Q

For each Clinical scenario below, choose the SINGLE most likely

D. To advise a patient on a method of reducing plasma cholesterol

  1. Measurement of body mass index and waist circumference
  2. Measurement of serum leptin concentration
  3. Measurement of resting energy expenditure
  4. Measurement serum polyunsaturated fat concentration
  5. Measurement of total plasma cholesterol and/or low density lipoprotein cholesterol concentration
  6. Oral ferrous sulphate
  7. Oral Folic acid
  8. Oral vitamin K
  9. Parenteral thiamine (Pabrinex)
  10. Reducing saturated fat and increasing mono or polyunsaturated fat in diet
A
  1. Reducing saturated fat and increasing mono or polyunsaturated fat in diet
172
Q

For each Clinical scenario below, choose the SINGLE most likely

E. To reduce risk of neural tube defect in woman seeking advice before pregnancy, with a previous pregnancy complicated by spina bifida in the infant.

  1. Measurement of body mass index and waist circumference
  2. Measurement of serum leptin concentration
  3. Measurement of resting energy expenditure
  4. Measurement serum polyunsaturated fat concentration
  5. Measurement of total plasma cholesterol and/or low density lipoprotein cholesterol concentration
  6. Oral ferrous sulphate
  7. Oral Folic acid
  8. Oral vitamin K
  9. Parenteral thiamine (Pabrinex)
  10. Reducing saturated fat and increasing mono or polyunsaturated fat in diet
A

7.Oral Folic acid

173
Q

What disorders are screened for by the heel prick spot test (5-9 days of life)?

A

Congenital hypothyroidism

Sickle cell disease

Cystic fibrosis

IMD:

Phenylketonuria

Medium Chain Acyl CoA Dehydrogenase deficiency

Homocystinuria

Isovaleric acidaemia

Maple syrup urine disease

Glutaric aciduria type 1

174
Q

What are some of the genetic causes of Rickets?

A

Pseudo vitamin D deficiency 1 - defective renal hydroxylation

Pseudo vitamin D deficiency 2 - Receptor defect

Familial hypophosphataemias - phosphate is needed for bone mineralisation and calcium absoption etc

175
Q

What are the 5 common problems associated with low birth weight babies?

A

Respiratory distress syndrome

Retinopathy of prematurity

Patent ductus arteriosus

Intraventricular haemorrhage

Necrotising enterocolitis

176
Q

What are some causes of jaundice presenting within the 1st 24 hours of life?

A

Pathological

Haemolytic diseases - Haemolytic anaemia, ABO incompatibility syndrome, Resus incompatibility syndrome

G6PD deficiency

Crigler-Najjar syndrome (defect in conjugation)

177
Q

What are some causes of prolonged jaundice?

A

Prenatal infection/sepsis/hepatitis

Hypothyroidism

Breast milk jaundice

178
Q

What period after birth is hypernatraemia common for?

A

1st 2 weeks of life

179
Q

What must you consider in cases where there is repetitive hypernatraemic episodes in a neonate?

A

Salt poisoning, osmoregulatory dysfunction

180
Q

What are the causes of hyponatraemia in a newly born neonate?

A

Excessive intake of water

SIADH secondary to infection i.e. a pneumonia or meningitis or intraventricular haemorrhage

Loss of sodium due to imature renal tubule function

Factitious i.e. due to hyperglycaemia

Congenital adrenal hyperplasia

181
Q

What is the most common deficiency causing congenital adrenal hyperplasia?

A

21-hydroxylase deficiency

182
Q

What is the precursor of cortisol that is elevated in congenital adrenal hyperplasia?

A

17- hydroxy pregnenolone

183
Q

At what level does bilirubin become free i.e. not bound to albumin?

A

Above 340 micromol/L

184
Q

Why are the NICE treatment thresholds for hyperbilirubinaemia much lower in premature infants compared to term infants?

A

They have a much lower albumin, so a higher proportion of bilirubin is free in the blood.

Their blood brain barrier is also more leaky. These 2 factors increase the chance of kernicterus.

185
Q

When does the fetus gain their calcium and phosphate from the mother?

A

Most occurs in the 3rd trimester, which explains why premature babies are at risk of osteopenia of prematurity

186
Q

What are porphyrias?

A

Porphyrias are a group of diseases that arise due to deficiencies in the enzymes of the haem biosythetic pathway.

These deficiencies in the enzymes within the pathway lead to a build up of toxic haem precursors/intermediaries.

187
Q

What are the 3 main presentations of porphyrias?

A

1) Acute neuro-visceral attacks - neurological sx, abdominal pain

Acute or chronic cutaneous sx - blistering (2), or non-blistering (3)

188
Q

What are the characteristics of haem?

A

Organic heterocyclic compound

Fe2+ in centre

4 pyrrolic (tetrapyrrole) rings around the iron

Carries oxygen

Redox reactions

Improtant for the erythroid cells and is a precursor of liver cytochrome

Made in all cells

189
Q

What is a structural difference between haem and its precursors?

A

Lack of a double covalent bond between the pyrrole rings in the precursors.

190
Q

An accumulation of what haem precursor causes a neurovisceral porphyria?

A

5-aminolaevulinic acid

191
Q

What does ALA synthase deficiency cause?

A

X-linked sideroblastic anaemia

192
Q

What must you remember when sending off a urine sample to a lab to check for suspected acute intermittent porphyria/ hereditary coproporphyria/ Protoporphyrinogen oxidase?

A

Protect the sample from light

193
Q

What’s the most common porphyria?

A

Porphyria cutanea tarda

194
Q

What is the most common porphyria in children and how does it present?

A

Erythropoeitic protoporphyria

Presents with: Non blistering, photosensitivity, burning, painful, itching and oedema after sun exposure

195
Q

What is the treatment for an erythropoeitic protoporphyria?

A

Tx: Sun avoidance

196
Q

How does porphyria cutanea tarda present?

A

Vesicles on sun-exposed areas of skin, superficial scarring, skin crusting and pigmentation

197
Q

What is the treatment for porphyria cutanea tarda?

A

Avoidance of precipitants: Drugs, alcohol, hepatic compromise (Hep B, HIV, cirrhosis)

198
Q

A 22 year old female comes back from her holiday where she had been drinking heavily. She now has abdominal pain, nausea and vomiting. Her family reports that she has also been paranoid.

Since her return she has experienced tonic/clonic seizures, blurred vision and flashing lights. She is admitted to a district general hospital.

Whats the potential diagnosis and what Ix would you do?

A

Ix: Pregnancy test.

Urine sample for porphobilinogen (PBG) - may be acute intermittent porphyria

199
Q

During acute porphyria, the most useful sample to send is….

a) Blood
b) CSF
c) Urine
d) Muscle biopsy
e) Stool
f) Skin biopsy

A

c) Urine

200
Q

What is the hyponatraemia associated with acute intermittent porphyria most likely due to?

A

SIADH

201
Q

Urine samples taken during an acute porphyria attack for diagnosis, should be:

a) taken in an acidified container
b) protected from light
c) alkalinised
d) interpreted with a paired serum sample

A

b) protected from light

202
Q

What are some side effects of T4 over replacement?

A

Osteopenia and atrial fibrillation

203
Q

A patient has a TSH of <0.01, Free T3 of 15.6 and Free T4 of 38.0. What is the likely diagnosis?

A

Thyrotoxicosis

204
Q

A patient has a TSH of 8.4, Free T4 of 11.7 and Thyroid peroxidase antibodies are positive, what is the diagnosis?

A

Subclinical hypothyroidism with later risk of hypothyroidism

205
Q

A patient has a TSH of 1.4 and free T4 of 12.1. What is the likely diagnosis?

A

Euthyroid status in a patient complaining of tiredness

206
Q

A patient has a TSH of 22.4 and free T4 of 6.3. What is the likely diagnosis?

A

Clinical primary hypothyroidism

207
Q

What is the normal range for TFTs?

A

TSH 0.33-4.5 mU/L

Free T3 3.2-6.5 pmol/L

Free T4 10.2-22.0 pmol/L

Thyroglobulin <5 ug/L

208
Q

A patient has a thyroglobulin of 254. What is the diganosis?

A

This is a test to screen for the recurrence of a differentiated thyroid carcinoma (papillary or follicular). As differentiated, functioning thyroid tissue produces thyroglobulin - so elevated levels would indicate the tumour is back. The most likely diagnosis would be recurrence of a papillary thyroid carcinoma as it is the most common type of thyroid cancer.

209
Q

How would we screen for medullary carcinoma of the thyroid?

A

Calcitonin levels or carcinoembryonic antigen levels (CEA)

210
Q

What is Lesch Nyhan syndrome?

A

It is a complete deficiency of HGPRT (Hypoxanthine Guanine Phosphoribosyl Transferase

211
Q

In purine metabolism…

a) The salvage pathway predominates over de-novo synthesis in most tissues
b) Xanthine oxidase oxidises xanthine to uric acid
c) HPRT is deficient in Lesch-Nyhan disease
d) PAT (PRPP Amido Transferase) is the rate limiting enzyme
e) PAT is under -ve feedback by AMP and GMP
f) All of the above

A

f) All of the above

212
Q

What are the different aims of acute and chronic gout?

A

Acute gout - reduce inflammation

Chronic gout - reduce plasma urate levels

213
Q

What are 2 different drug types used to manage hyperuricaemia in chronic gout?

A

1) Xanthine oxidase inhibitors (allopurinol) - these prevent the production of xanthine and uric acid from hypoxanthine
2) Uricosuric drugs (Probenecid) - increases renal excretion of urate

214
Q

In the treatment of acute gout…

a) Allopurinol should be used acutely
b) NSAIDs are the first line tx in acute attacks
c) Colchicine lowers urate levels
d) Allopurinol lowers urate levels by inhibiting HPRT
e) Allopurinol lowers urate levels by inhibiting xanthine oxidase

A

b) NSAIDs are the first line tx in acute attacks and
e) Allopurinol lowers urate levels by inhibiting xanthine oxidase

215
Q

On aspiration and microscopy of the synovium of a joint, there is a neutrophil containing needle shaped yellow-orange crystals in the direction of the red compensator. With one crystal perpendicular to this which is a blue colour. What is the likely crystal type?

a) -vely birefringent urate crystal
b) +vely birefringent urate crystal
c) +vely birefringent pyrophosphate crystal
d) Rheumatoic arthritis
e) Gonococcal arthritis

A

a) -vely birefringent urate crystals

216
Q

On aspiration and microscopy of the synovium of a joint, there is a neutrophil containing elongated rectangular-oval shaped blue crystals in the direction of the red compensator. What is the likely crystal type?

a) -vely birefringent urate crystal
b) +vely birefringent urate crystal
c) +vely birefringent pyrophosphate crystal
d) Rheumatoid arthritis
e) Gonococcal arthritis

A

c) +vely birefringent pyrophosphate crystal - found in pseudogout

217
Q

What is the criteria for hyperosmolar hyperglycaemic state (HHS)?

A

Hypovolaemia

Glucose > 30mmol/L

No ketonaemia

Osmolality > 320 mOsmol/kg

218
Q
A

Pathology Amber (6 decks)

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