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4th year everything > Biochemistry AS > Flashcards

Biochemistry AS Flashcards

1
Q

What would you see on bloods in dehydration?

A

Increased urea, creatinine
Increased albumin
Increased haematocrit

Disproportionately increased urea to creatinine.

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2
Q

What would you see in a low GFR?

A 
Increased Urea
Increased Creatinine 
Increased H+ 
Increased Potassium 
Increased PO4
Decreased Ca
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3
Q

Tubular dysfunction

A

Normal U and Cr

Decreased K, decreased Urate, decreased PO4, decreased HCO3.

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4
Q

What would you see in thiazide and loop diuretics (furosemide)

A

Decreased Sodium
Decreased Potassium
Increased HCO3
Increased Urate

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5
Q

Hepatocellular Disease views?

A

ETOH = AST:ALT>2, increased GGT

Viral = AST: ALT <2

Increased bilirubin, increased ALP, decreased albumin, increased PT (APTT increased if end-stage).

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6
Q

Cholestasis on blood test?

A

Increased ALP, increaseD GGT, increased bilirubin, increased AST.

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7
Q

Excess EtOH intake blood test levels?

A

Increased GGT, Increased MCV, evidence of hepatocellular disease.

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8
Q

Addison’s disease bloods?

A

Increase potassium, decreased Na

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9
Q

Cushing’s Disease bloods?

A

May show: decreased K, Increased sodium, increased HCO3

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10
Q

Conn’s disease bloods?

A

Decreased K
Increased Na
Increased HCO3

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11
Q

Diabetes insipidus bloods?

A

Increased sodium
Increased serum osmolality
Decreased urine osmolality

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12
Q

SIADH bloods?

A

Patient presents with hyponatraemia, then to check osmolality of the urine,

Decreased sodium
Decreased serum osmolality
Increased urine osmolality
Increased Urine Na

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13
Q

Hyponatremia - levels and symptoms

A

<135: n/v, anorexia, malaise
<130: headache, confusion
<125: seizure, non-cardiogenic pulmonary oedema
<115: coma and death

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14
Q

What are the causes of hypovolaemic hyponataemia

A

U Na > 20nM (= renal loss)

  • Diuretics
  • Addison’s
  • Osmolar diuresis (e.g glucose)
  • Renal failure (diuretic phase)

U Na < 20mM (extra-renal loss)

  • Diarrhoea
  • Vomiting
  • SBO
  • Burns
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15
Q

What are the causes of hypervolaemic hyponatraemia

A

Cardiac failure
Nephrotic syndrome
Cirrhosis
Renal failure

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16
Q

Euvolaemic hyponatraemia?

A

U osmolality >500 - SIADH

U osmolality <500 - Water overload, severe hypothyroidism, glucocorticoid insufficiency

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17
Q

Management of Hyponatraemia?

A

Correct underlying cause

  • Replace Na and water at the same rate they were lost. Beware if you replace too fast you get central pontine myelinolysis.
  • Chronic: 10mM/d
  • Acute: 1mM/hr.

Low to high, pons will die
High to low, brain will blow.

Normally <0.5mmol/hr.

Asymptomatic chronic hyponatraemia
- Fluid restrict

Symptomatic/acute hyponatremia/dehydrated
- Caution rehydration with 0.9% saline.

If hypervolaemic consider frusemide

Emergency: seizure, coma
- consider hypertonic saline. (1.8%).

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18
Q

What is SIADH?

A

Concentrated urine: Na >20mM, osmolality >500.

Hyponatraemia or plasma osmolality <275.

Absence of hypovolaemia, oedema, or diuretics.

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19
Q

Causes of SIADH?

A

Resp: SCLC, pneumonia, TB
CNS: meningoencephalitis, head injury, SAH
Endo: hypothyroidism
Drugs: cyclophosphamide, SSRI, CBZ

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20
Q

Management of SIADH?

A

Treat cause and fluid restrict

Vasopressin receptor antagonist

  • Demeclocycline
  • Vaptans
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21
Q

Hypernatraemia presentation?

A 
Thirst
Lethargy
Weakness
Irritability
Confusion, fits, coma
Signs of dehydration

In children can lead to cerebral shrinkage. Can be due to dehydration, profuse, low-sodium diarrhoea.

Manage w

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22
Q

Causes of hypovolaemic hypernatraemia

A

GI Loss: diarrhoea, vomiting
Renal loss: diuretics, osmotic diuresis
Skin: Sweating, burns

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23
Q

Causes of euvolaemic hypernatraemia?

A

Decreased fluid intake
DI
Fever

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24
Q

Causes of hypervolaemic hypernatraemia ?

A
  • Hyperaldosteronism (Increased BP, decreased K, alkalosis)

- Hypertonic saline.

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25
Q

Investigation of Hypernatraemia?

A

Increased Na
Dilute Urine
Dx: Water deprivation test

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26
Q

Management of hypernatraemia

A

Treat cause.

Manage with slow infusion over 48 to reduce risk of cerebral oedema.
Desmopressin if cranial.

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27
Q

Symptoms of hypokalaemia?

A 
Muscle weakness
Hypotonia
Hyporeflexia
Cramps 
Tetany
Palpitations
Arrhythmia

NB: decreased potassium exacerbates digoxin toxicity

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28
Q

ECG findings of Hypokalaemia?

A

Results from delayed ventricular repolarisation

  • Flattened /inverted T waves
  • Prominent U waves (after T waves)
  • ST depression
  • Long PR interval
  • Long QT interval.
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29
Q

Causes of hypokalaemia?

A

Alkalosis
Increased insulin
B-agonists

Increased excretion

  • GI: vomiting, diarrhoea, rectal villous adenoma
  • Renal: RTA (esp Type 2), Bartter syndrome
  • Drugs: diuretics, steroids
  • Endo: Conn’s syndrome , Cushing’s syndrome

Decreased input
- Inappropriate IV fluid management

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30
Q

Management of general hypokalaemia?

A
  • 1mM K = 200-300mmol total deficit
  • Don’t give K if oliguric
  • Never give STAT fast bolus
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31
Q

Management of mild hypokalaemia?

A

K >2.5

  • Oral K supplements
  • > 80mmol/d.
Severe: K<2.5 and/or dangerous symptoms 
- IV KCL cautiously 
- 10mmol/h (20mmol/h max) 
- Give centrally (burning sensation peripherally) 
Max central conc: 60mM 
Max peripheral conc: 40mM

Mg replacement

  • Pts are often Mg deplete too
  • Until Mg is replaced the K will not return to normal levels despite K replacement
  • Give empiric Mg Replacement.
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32
Q

Symptoms of hyperkalaemia?

A

Fast, irregular pulse
Palpitations
Chest pain
Weakness

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33
Q

SIgns of hyperkalaemia?

A 
Tall tented T waves 
Flattened P waves
Increased PR interval
WIdened QRS
Sine-wave pattern --> VF
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34
Q

Causes of Hyperkalaemia?

A

Artefact

  • Haemolysis
  • K2EDTA contamination from FBC bottles
  • Leucocytosis, thrombocytosis
  • Drip arm

Internal distribution

  • Acidosis
  • Decreased insulin
  • Cell death/tissue trauma/burns
  • Digoxin poisoning
  • Suxamethonium
Decreased excretion 
- Oliguric renal fialure 
- Addison's 
- Drugs: 
ACEi, 
NSAIDs, 
K-sparing diuretics (spiro) 
Heparin (inhibition of aldosterone secretion)

Increased input

  • Excessive K therapy
  • Massive transfusion
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35
Q

Management of hyperkalaemia?

A

Non-urgent

  • treat cause: review meds
  • Polystyrene sulphonate resin: Binds K in the GIT and decreased K over days.

Emergency: Evidence of myocardial instability or K >6.5

  • 10ml 10% calcium gluconate
  • 100ml 20% glucose + 10u insulin (actrapid)
  • Salbutamol 5mg nebuliser
  • Haemofiltration
  • Calcium resonium 15g PO or 30g PR.
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36
Q

How does PTH affect Ca and PO4?

A

Increased Ca
Decreased PO4

Ionised Ca –> PTH release.

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37
Q

Renal effect of PTH?

A
  • Increased Ca
  • Decreased PO4 resorption
    Increased 1a-hydroxylation of 25-OH Vit D3 in kidney
  • Increased HCo3 excretion (may –> mild met acidosis)
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38
Q

Bone effects of PTH?

A

Increased osteoclast activity –> increased Ca, increased PO4.

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39
Q

Vitamin D and Calcitriol role?

A

Hepatic 25 hydroxylation -_> 25-OH Vit D3 (calcidiol)

Renal 1a-Hydroxylation in kidney –> 1,25 (OH)2 Vit D3
- Increased by increased PTH, decreased Ca, decreased PO4.

40
Q

Gut effect of PTH?

A
  • Increased Ca and increased PO4 absorption

- Inhibition of PTH release

41
Q

Magnesium effect of PTH?

A

decreased Mg prevents PTH release

- May –> Decreased Ca.

42
Q

Plasma binding 2.2-2.6mM for calcium?

A

50% Albumin bound (decreased albumin –> decreased Ca).
- Alkalosis –> decreased albumin protonation –> increased Ca binding -> Decreased free Ca.

Therefore prolonged tourniquet application –> increased albumin –> increased Ca.

43
Q

What is the presentation of hypocalcemia?

A

Spasms (Carpopedal = Trousseau’s sign (inflate BP cuff) - Wrist flexion and fingers drawn in.
Anxious, irritable
Seizures
Muscle tone increased: colic, wheeze, dysphagia
Orientation impaired (confusion)
Dermatitis: atopic, exfoliative
Impetigo herpetiformis (decreased Ca + pustules )
Chovsteks, Cardiomyopathy (increased QTc –> TdP) - Tapping over parotid causes facial muscle to twitch.

44
Q

Causes of hypocalacaemia?

A

Commonest cause is CRF.

  • With increased PO4

CKD, hypoparathyroidism, decreased Mg, acute rhabdomyolysis.

  • With normal or decreased Po4
    Osteomalacia
    Active pancreatitis
    respiratory alkalosis
45
Q

Management of hypocalcaemia?

A

Mild

  • Ca 5mmol QDS PO
  • Daily Ca levels

CKD
- Alfacalcidol (1-OH- Vit D3

Severe

  • 10ml 10% Ca gluconate IV (2.25 mmol over 30 mins)
  • repeat as necessary.
46
Q

Hypercalcaemia presentation?

A

Stones, bones, moans, groans.

  • May also have increased Bp (Check Ca in all with HTN)
  • Decreased QT interval.
47
Q

Causes of hypercalcaemia?

A

Most commonly malignancy or primary HPT.

48
Q

Hypercalcaemia with increased PO4 and increased ALP?

A

Increased bone turnover?

  • Bone mets (breast, lung, kidney, prostate, colon)
  • Sarcoidosis
  • Thyrotoxicosis (bone metabolism)
  • Lithium
49
Q

Hypercalcaemia with normal ALP, increased PO4?

A

Myeloma
Hypervitamonosis D
Sarcoidosis
Milk alkali syndrome

50
Q

Hypercalcaemia with normal or decreased PO4?

A

primary or tertiary HPT
Familial benign hypercalciuria
Paraneoplastic: PTHrP (but decreased PTH)

51
Q

Investigations of hypercalcaemia?

A

Increased PTH = primary or tertiary PTH
Decreased PTH = most likely Ca
FBC, protein electrophoresis, CXr, bone scan.

52
Q

Management of hypercalcaemia?

A

rehydrate

  • 1L 0.9% saline/4hrs
  • Monitor pts hydration state

Frusemide

  • Only start once pt is volume replete
  • Calciuric + makes room for more fluids

Bisphosphonates
- Ca bisphosphonate can’t be resorbed by osteoclasts
- Only use in hypercalcaemia of malignancy
(Can obscure Diagnosis -> Ca decreased ,Po4 decreased and PTH increased)
- Takes 2-3 days to work with maximal effect.
- Pamidronate, Zoledronate (IV).

Give advise about good hydration (as long as no impairment)

  • Reassure that a low calcium diet is not necessary.
  • Advise person to avoid any drugs or supplements that could exacerbate.
  • Encourage mobilisationation
  • Advise them to report any hypercalcaemia
53
Q

Osteoporosis types?

A

Decreased Bone mass

Primary: age related
Secondary: Drug or other conditions

54
Q

Risk factors for osteoporosis?

A 
Steroids 
Hyperthyroidism, HPT, HIV
Alcohol and Cigarettes
Thin (BMI <22) 
Testosterone low 
Early menopause
Renal/liver failure 
Erosive/inflammation bone disease (RA, myeloma) 
Dietary Ca 
low/malabsorption

FRAX looks at

  • history of glucocorticoid use
  • RA
  • Alcohol excess
  • History of parental hip fracture
  • low BMI
  • current smoking
55
Q

Presentation of osteoporosis?

A

Vertebral Crush fracture

NOF or other long bone fractures

56
Q

Investigations for osteoporosis?

A

Bone profile, FBC, U+E

DEXA. Liver test, CRP, TFTs.

57
Q

DEXA Scan results?

A

Indications

  • Low-trauma #
  • women >65yrs with one or more risk factor
  • Before giving long-term steroids >3months)
  • Parathyroid disorders, myeloma, HIV.
58
Q

Interpretation of DEXA scan?

A

T: no of SDs away from youthful average
Z: no. of SD away from matched average.

T>-1 = normal
T -1 - -2.5 = osteopenia
T

59
Q

Management of Osteoporosis?

A
  • Decision to instigate pharmacological management is based upon age, RFs, and BMD
  • FRAX can estimate 10yr #rish.

Conservative

  • stop smoking, decreased ETOH
  • Weight bearing or balancing exercise (tai Chi)
  • Ca and vit D rich diet.
  • Home-based fall-prevention program with visual assessment.
60
Q

Primary and secondary prevention of fractures in osteoporosis?

A

Bisphosphonates: alendronate is 1st line
Zolendronic acid is IV and if you can’t tolerate oral.

Ca and Vit D supplements: e.g calcium D3, Forte.

Strontium ranelate: bisphosphonate alternative.
- Dual action bone agent. Promotes osteoblasts, inhibits osteoclasts. Only taken if no other treatment for osteoporosis. Can cause SJS.

61
Q

Alternatives for secondary prevention of osteoporotic fractures?

A

If they cannot take alendronate because of age, T-score, number of risk factors (parental history of hip fracture, alcohol intake of 4 or more units per day, RA).

Raloxifen: SERM, decreased Breast Ca risk with HRT.

Terparetide: PTH analogue –> new bone formation

Rarely given: Denosumab: Anti-RANKL –> Decreased osteoclast activity.

62
Q

Bisphosphonate SEs

A
  • GI upset
  • Oesophageal ulceration/erosion
  • Diffuse musculoskeletal pain
  • Osteonecrosis of the jaw.
63
Q

What is osteomalacia?

A

Decreased bone mineral content
- Excess uncalcified osteoid and cartilage

RF
- Vegan, breast milk, malabsorption, CLD, CRD.

64
Q

Presentation of osteomalacia?

A

children = Rickets

  • Knock-kneed
  • Bone pain
  • Craniotabes-
  • Osteochondral swelling; Rachitic rosary
  • Harrison’s sulcus.

Osteomalacia: adults (after epiphyseal fusion)

  • Bone pain and tenderness
  • fractures (NOF)
  • Proximal myopathy due to decreased PO4.
65
Q

What are the causes of osteomalacia?

A
  • Vit D deficiency: malabsorption, poor diet, decreased sunlight
  • Renal osteodystrophy: decreased 1a hydroxylation
  • Drugs: AEDs –> Increased hepatic Vit D metabolism.
  • Vit D resistance
  • Hepatic disease: malabsorption and decreased 25 hydroxylation

Malignancy: oncogenic hypophosphataemia
- increased fibroblast growth factor-23 – >hyperphosphatemia

66
Q

What are the investigations for osteomalacia?

A 
Decreased Ca
Decreased PO4 
Increased ALP
Increased PTH
Decreased 25-OH Vit D (unless resistance)

X-ray
= Loss of cortical bone
- Looser’s zones: pseudofractures
- Cupped metaphyses in Rickets.

67
Q

Management of osteomalacia?

A

Dietary: Calcium D3 Forte
Malabsorption or hepatic disease
- Vit D2 PO (ergocalciferol)
- Parenteral calcitriol

Renal disease or Vit D resistance

  • 1a-OH Vit D3 (alfacalcidol)
  • Decreased 1-25(OH)2 Vit D3 (calcitriol)

Monitor Plasma Ca

68
Q

What is Paget’s Disease?

A

Increased bone turnover – bone remodelling, enlargement + weakness.

69
Q

Phases of Paget’s disease?

A

Osteolytic
Mixed Osteolytic-osteoblastic
Quiescent osteosclerotic stage

70
Q

Presentation of Paget’s disease?

A

Asymptomatic in 70%
Predominantly affects the axial skeleton
- Pelvis, lumbar spine, skulls, femur, tibia

Bone pain
Patholgical fracture
Deformity
Head enlargemet

71
Q

Complications of Paget’s disease?

A
  • Nerve compression: deafness ,radiculopathy
  • High output CCF
  • Osteosarcoma (<1% after 10yrs)
72
Q

Investigations of Pagets?

A

Very high ALP (ca and po4 normal)

Bone scan: hot spots

X-ray = Bone enlargement, sclerosis, patchy cortical thickening
- wedge-shaped lytic lesions,
Osteoporosis circumscripta - well defined lytic skull lesions.

73
Q

Management of paget’s

A

Analgesia

Alendronate: Decreased pain and or deformity.

74
Q

Osteoporosis biochem?

A

Everything normal

75
Q

Osteomalacia biochem?

A

Ca low
PO4 low
ALP high
PTH high

76
Q

Primary HPT cause?

A

Parathyroid adenoma or hyperplasia.

Hypercalcaemia

  • Bloods =
    High PTH, High Calcium, low PO4.High ALP.
77
Q

Secondary HPT cause?

A

Chronic renal failure
Vit D deficiency
Malabsorption

Bloods
- High PTH, Low calcium, high PO4, high ALP

78
Q

Tertiary HPT cause?

A

Parathyroid hyperplasia due to prolonged 2ndry HPT?

  • High calcium, high PO4, high ALP, high PTH.
79
Q

Characteristics of HPT?

A

Osteitis fibrosa cystica

  • Subperiosteal erosions
  • Acral osteolysis
  • Cysts
  • Brown tumours
  • Pepperpot skull
80
Q

Hypo PTH?

A

Low Ca, high PO4, normal ALP, Low PTH.

81
Q

Renal osteodystrophy?

A

PO4 retention + low Vit D –> decreaseD Ca –> increased PTH.

Osteomalacia, osteosclerosis, osteoporosis.

82
Q

Types of Hyperlipidaemia?

A

Common primary hyperlipidaemia

Familail primary hyperlipiaemia

2ndry hyperlipidaemia - increased LDL (nephrotic syndrome, hypothyroidism, Cushings) or mixed due to T2DM, ETOH.

83
Q

Familial Primary Hyperlipidaemia

A

Primary hypercholesterolaemia
- ApoB (LDL receptor defect = increased LDL. AD disoder caused by a mutation in the gene coding the low-density lipoprotein LDL receptor. Causes early-onset hypercholesterolaemia.
FH = xanthelasma, tendon xanthoma, corneal arcus, raised cholesterol and LDL.

Combined hyperlipiaemia
- LDL increased + increased TG

Lipoprotein lipase deficiency
- Increased Chylomicrons

84
Q

Presentation of hyperlipidaemia?

A

CVD, xanthomata (eruptive, tuberous at elbows, knees, planar - ornage streaks in palmer creases, xanthalesma: eyelids

Pancreatitis.

85
Q

Management + Aims of hyperlipidaemia

A

Aim TC: <4
TC:HDL ratio <4.5

1st line

  • Statins - Simvastatis 40mg PO node
  • HMG-CoA

Can also use: Fibrates, PPARalpha antagonist

Ezetimibe: inhibits cholesterol absorption

Niacin/nicotinic acid: increased HDL, Decreased LDL.

86
Q

Acute INtermittent Porphyria

A

GI pain, constipaiton, CV: increased HR, BP.

Neuropsych + red urine.

Precipitants = P450 inducer, stress, infection.

INcreased Urine PBG and ALA.

Manage with supportive anaglesia, IV fluids, carbohydrate.

Can give IV haematin.

87
Q

Porphyria Cutanea Tarda

A

Commonest porphyria
Only cutaneous manifestation

  • Photosensitivity: blistering skin lesions
  • Facial hyperpigmentation
  • Increased urine + se porphyrins
  • Increased se ferritin

Avoid sun, phlebotomy/iron chelators.

Cholorquine.

88
Q

Hyperlipidaemia secondary cause leading to a predominately hypertriglyceridemia?

A 
DM (T1+2) 
Obesity
Alcohol
Chronic renal failure 
Drugs: thiazides, non-selective beta-blockers, unopposed oestrogen.
89
Q

Hyperlipidaemia secondary cause leading to a predominately hypercholesterolaemia?

A

Nephrotic syndrome
Cholestasis
Hypothyroidism

90
Q

Hypophophataemia

A

Can be caused by DKA

Phosphate 0.65-0.81 = Mild
0.32-0.65 = Moderate
<0.32 = Severe

Rise in insulin causes phosphate to shift into intracellular compartment.

Other causes:

  • Alcohol excess
  • Acute liver failure
  • DKA
  • refeeding syndrome
  • Primary hyperparathyroidism
  • Osteomalacia

Consequences

  • red blood cell haemolysis
  • White blood cell and platelet dysfunction
  • Muscle weakness + rhabdo
  • CNS dysfunciton.

Management
- Continue with current insulin therapy and initiate parenteral phosphate replacement.

91
Q

Treatment of hyperuricaemia?

A

No treatment to prevent gout.

Gout is associated with high level of uric acid however it is possible to have hyperuricaemia without any noticeable effects.

Recommend against primary prevention of gout.

92
Q

Hyperuricaemia?

A

Increased levels of uric acid may be seen secondary to either increased cell turnover or reduced renal excretion of uric acid. Hyperuricaemia may be found in asymptomatic patients who have not experienced attacks of gout

Hyperuricaemia may be associated with hyperlipidaemia and hypertension. It may also be seen in conjunction with the metabolic syndrome

Increased synthesis
Lesch-Nyhan disease
myeloproliferative disorders
diet rich in purines
exercise
psoriasis
cytotoxics
Decreased excretion
drugs: low-dose aspirin, diuretics, pyrazinamide
pre-eclampsia
alcohol
renal failure
lead
93
Q

ALP raised and raised calcium?

A

Bone mets

Hyperparathyroidism

94
Q

ALP raised and low calcium

A

Osteomalacia

Renal failure

95
Q

Causes of raised ALP?

A

liver: cholestasis, hepatitis, fatty liver, neoplasia
Paget’s
osteomalacia
bone metastases
hyperparathyroidism
renal failure
physiological: pregnancy, growing children, healing fractures

4th year everything (43 decks)

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