Biochemistry Flashcards

(64 cards)

1
Q

What do U&E measure:

A
Electrolytes (Potassium and Sodium) 
Renal function (Urea and Creatinine)
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2
Q

Hyponatraemia Sodium level

A

Less than 135mmol/L

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3
Q

What is important to look at for hyponatraemia

A

Osmalality: this is lower in true hyponatraemia

Volume status

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4
Q

Causes of hypovolaemia hyponatraemia

A

Vomiting, Diarrhoea

Renal: Diuretics (K sparing), Nephropathy (PKD, NAIDs, pyelonephritis), Adrenal insufficiency/Addison’s

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5
Q

Causes of isovolaemic hyponatraemia

A

SIADH (high urine osmolality assoc)
Drugs
Renal failure / AKI
Hyperthyroidism

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6
Q

Causes of hypervolaemic hyponatraemia

A

Liver failure
Congestive heart failure (fluid overload)
Renal failure / AKI
Nephrotic syndrome

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7
Q

Causes of hypernatraemia

A

Diabetes insipidus (Polydispsia and polyuria causes fluid and salt loss)

Poor water intake (e.g. elderly, bed bound)

Too much IV sodium

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8
Q

Hypokalaemia level

A

Potassium less than 3.5

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9
Q

Causes of hypokalaemia

A

Drugs: Diuretic (e.g Thiazides - Indapamide), Tx DKA

GI: D&V, high stoma output

Renal: renal tubular acidosis or drug induced renal damage

Endocrine: Metabolic acidosis

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10
Q

Causes of hyperkalaemia

K over 6.5 - this is a medical emergency needing an ECG monitoring and Tx

if less than 6.5 then Tx needed if ECG is abnormal

A

Renal failure / AKI (And also missing dialysis appt)

Drugs: K sparing (Spironolactone), Potassium supps

Rhabdomyolysis, DKA

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11
Q

ECG changes in hypokalaemia

A

Flat broad T-waves
ST-depression
Long QT
Ventricular dysrhythmia

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12
Q

ECG changes in hyperkalaemia

A

Tall-tented T-waves (moving to Sine-wave - this is very severe stage)
Loss of P
QRS broadening
Cardiac arrest rhythms

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13
Q

What needs to be looked at for creatinine

What takes this into account

A

Age, sex and muscle bulk.

An old thin lady with normal range creatinine may be in renal failures this is high for her.

eGFR

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14
Q

Ways of predicting GFR

A

eGFR

Creatinine clearance

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15
Q

What does osmolarity take into account

A

U&Es

Blood Glucose

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16
Q

What factors determine nutritional profile

A

Magnesium
Calcium
Phosphate
Albumin

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17
Q

Refeeding syndrome

A

Insulin release causes increased glycogen, fat and protein synthesis.

This requires magnesium, phosphate and potassium which are already depleted

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18
Q

Urine in Pre-renal AKI (hypoperfusion) Vs Renal AKI from ATN

A

In pre-renal the urinary sodium is low as Juxtaglomerular apparatus is function and can activate RAAS

In Renal AKI from ATN urinary sodium is high due to breakdown in physiological mechanisms

Similarly in pre-renal uraemia, Urine will be more concentrated than in ATN

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19
Q

Ways of predicting GFR

A

eGFR

Creatinine clearance

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20
Q

What does osmolarity take into account

A

U&Es

Blood Glucose

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21
Q

What factors determine nutritional profile

A

Magnesium
Calcium
Phosphate
Albumin

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22
Q

Refeeding syndrome

A

Insulin release causes increased glycogen, fat and protein synthesis.

This requires magnesium, phosphate and potassium which are already depleted

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23
Q

Urine in Pre-renal AKI (hypoperfusion) Vs Renal AKI from ATN

A

In pre-renal the urinary sodium is low as Juxtaglomerular apparatus is function and can activate RAAS

In Renal AKI from ATN urinary sodium is high due to breakdown in physiological mechanisms

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24
Q

What needs to be looked at for creatinine

What takes this into account

A

Age, sex and muscle bulk.

An old thin lady with normal range creatinine may be in renal failures this is high for her.

eGFR

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25
Ways of predicting GFR
eGFR | Creatinine clearance
26
What does osmolarity take into account
U&Es | Blood Glucose
27
What factors determine nutritional profile
Magnesium Calcium Phosphate Albumin
28
Refeeding syndrome
Insulin release causes increased glycogen, fat and protein synthesis. This requires magnesium, phosphate and potassium which are already depleted
29
Urine in Pre-renal AKI (hypoperfusion) Vs Renal AKI from ATN
In pre-renal the urinary sodium is low as Juxtaglomerular apparatus is function and can activate RAAS In Renal AKI from ATN urinary sodium is high due to breakdown in physiological mechanisms
30
Components of Bone Profile
Calcium Phosphate Alk Phosphatase Albumin (Other factors: PTH, Vit D)
31
PTH actions
(released due to low calcium) Increased Calcium reabsorption from bone Increased renal calcium reabsorption Increased renal excretion of phosphate Inc absorption of Ca from gut (Vit D mediated)
32
Osteoporosis Calcium Phosphate ALP
Calcium Normal Phosphate Normal ALP Normal
33
Osteomalacia Calcium Phosphate ALP
Calcium Reduced Phosphate Reduced ALP Increased
34
Pagets Calcium Phosphate ALP
Calcium Normal Phosphate Normal ALP Increased
35
Mets Calcium Phosphate ALP
Calcium Increased Phosphate Increased ALP Increased
36
Primary hyperPTH (from PTH overactivity) Calcium Phosphate ALP
Calcium Increased Phosphate Decreased ALP Increased
37
Secondary hyperPTH (due to vitamin D def) Calcium Phosphate ALP
Calcium Low Phosphate Increased ALP Increased
38
Tertiary hyperPTH (due to renal failure) Calcium Phosphate ALP
Calcium Increased Phosphate Decreased ALP increased Differentiated from Primary with Hx of renal impairment
39
Causes of hypercalcaemia
Bone mets Multiple Myeloma Hyperparathyroidism Excessive Vit D
40
Seven Factors to test in LFTs
``` Bilirubin AST (not liver specific - muscle damage) ALT ALP (not liver specific - bone turnover) GGT Albumin PT ```
41
Autoimmune hepatitis test and result
Autoanitbody screen ANA Anti-smooth muscle Anti-microsomal
42
PBC test
Anti-mitochondrial antibody
43
Coeliac test
Anti-Tissue Transglutaminase
44
Haaemochromatosis biochem
High Iron, ferritin and transferrin saturation | Low TIBC
45
Wilson's disease biochem
Low Caeruloplasmin and elevated 24 hour urine copper conc
46
HCC biomarker
Alpha-Fetoprotein
47
Hepatocellular pattern of LFT dysfunction
Transaminitis (AST and ALT raised)
48
Obstructive pattern of LFT dysfunction
Elevated ALP and GGT Bilirubin also high (in severe cases AST and ALT may also rise due to back pressure in liver although not as much as ALP and GGT)
49
Causes og hepatocellular damage
``` Viral hepatitis Autoimmune hepatitis Drugs and toxins Alcohol Metabolic (Haemochromatosis, Wilson) NAFLD Malignancy (primary and mets) Congestive cardiac failure ```
50
Tumour markers: Colorectal
Carcinoembryonic antigen
51
Albumin and inflammation
Albumin is negative acute phase protein as it goes down in inflammation
52
What is CRP
Produced in Liver | Acute phase protein: high in infection and inflammation
53
When is ESR high and CRP normal
SLE | Multiple Myeloma
54
Uric acid metabolism
Produced during metabolism of purines and excreted by kidneys
55
Causes of high urate
Increased consumption of purines Impaired uric acid excretion (this is what causes gout - acute mono arthritis)
56
Tumour markers: HCC
Alpha-Fetoprotein
57
Tumour markers: Testicular teratoma, seminoma, choriocarcinoma
Human chorionic gonadotropin
58
Tumour markers: Prostate ca
PSA
59
Tumour markers: Ovarian
Ca-125
60
Tumour markers: Pancreatic Ca
Ca-19-9
61
Tumour markers: Colorectal
Carcinoembryonic antigen
62
Cause, Symptoms & Test for Cystic Fibrosis
Mutation in the gene for Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) responsible for Chloride transport across epithelial cells Causes viscous secretions in lungs and pancreas and also infertility Sweat test (Over 60mmol/L Chloride)
63
Fluid balance: E.g. of fluid entering the body
Food and drink IV Enteral or parenteral nutrition Blood products
64
Fluid balance: E.g. of fluid leaving the body
``` Urine Bowel motions Blood loss Fluid from drains e.g. chest drain Insensible losses (expired and sweat) - 500ml/day (higher in burns, fever etc) ```