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Path 2022 > Chem Path > Flashcards

Chem Path Flashcards

1
Q

Normal blood pH

A

7.35-7.46

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2
Q

Causes of metabolic acidosis

A

o Increased H+ production e.g., DKA
o Decreased H+ excretion e.g., renal tubular acidosis
o Bicarbonate loss e.g., intestinal fistula

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3
Q

Causes of respiratory acidosis

A

o Decreased ventilation
o Poor lung perfusion
o Impaired gas exchange

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4
Q

Causes of metabolic alkalosis

A

o H+ loss e.g., pyloric stenosis
- Also a raised urea, creatinine, total protein (dehydration)
- Low potassium, low chloride
o Hypokalaemia
o Ingestion of bicarbonate

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5
Q

Causes of respiratory alkalosis

A

Hyperventilation due to:

o Voluntary e.g., anxiety
o Artificial ventilation
o Stimulation of respiratory centre

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6
Q

Cystic Fibrosis diagnostic Ix (in neonate)

A

High blood immune reactive trypsin (IRT)

If IRT >99.5th centile in 3 bloodspots –> do 4 panel DNA mutation analysis
• 2 mutations = CF
• 1 mutation = 28 panel analysis
• 0 mutations = may repeat IRT at 21-28 days if IRT>99.9th centile

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7
Q

Specificity & sensitivity calculations

A

Sensitivity = true positive / total disease present

Specificity = true negative / total disease absent

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8
Q

Predictive value calculations

A

Positive predictive value = true positive / total positive
- NOTE: PPV depends on disease prevalence/incidence too!

Negative predictive value = true negative / total negative

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9
Q

Presentation of Organic Acidurias in neonate

A 
Unusual odour e.g. cheesy/sweaty smell (in isovaleric academia)
Lethargy
Feeding problems
Truncal hypotonia / limb hypertonia
Myoclonic jerks
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10
Q

Differences in neonatal kidneys

A

Low GFR for surface area:

  • slow excretion of solute load
  • limited Na+ available for H+ exchange

Short proximal tubule –> low reabsorptive capability (but is usually enough for small filtered load)

Short Loops of Henle/distal collecting duct –> reduced ability to concentrate urine

Distal tubule relatively unresponsive to aldosterone –> persistent loss of Na+

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11
Q

Causes of Hypernatraemia in neonates

A

Uncommon after 2 weeks

Usually dehydration

Rare causes:

  • Salt poisoning
  • Osmoregulatory dysfunction
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12
Q

Most important cause of HYPOnatraemia in neonate

A

Congenital adrenal hyperplasia

lack of 21 hydroxylase

  • -> build up of 17-OH progesterone
  • -> absence of aldosterone + cortisol
Signs/Sx:
o	Hyponatraemia
o	Hyperkalaemia
o	Marked volume depletion
o	(+ hypoglycaemia)
o	Ambiguous genitalia in female neonates
o	Growth acceleration in older child
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13
Q

Causes of high UNCONJUGATED bilirubin in neonate

A

Early rise:

  1. High level of synthesis (RBC breakdown)
    - Haemolytic disease – ABO, Rhesus incompatibility
    - G6PD deficiency
    - Crigler-Najjar syndrome
  2. Low rate of transport into liver and 3. Enhanced enterohepatic circulation
    - Biliary atresia, choledocal cyst
    - Ascending cholangitis in TPN
    - Inherited metabolic disorders

Prolonged jaundice (<14 in term, >21 in preterm)

  • Prenatal infection / sepsis / hepatitis
  • Hypothyroidism – screened at day 6-8 (Guthrie?)
  • Breast milk jaundice
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14
Q

Key features Acute intermittent porphyria

A

Neurovisceral attacks

  • abdo pain
  • SIADH & hyponatraemia
  • seizures
  • sensory loss / muscle weakness

NO SKIN LESIONS

Precipitated by:

  • medications: barbiturates, steroids, anti-convulsants
  • alcohol
  • stress: surgery, infection
  • reduced calorie intake
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15
Q

Other Acute porphyrias (not acute intermittent)

A

Hereditary Coproporphyria
Variegate Porphyria

Both have acute neurovisceral attacks + skin lesions

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16
Q

Non-acute porphyrias

A

Congenital eryrthopoietic porphyria

  • only skin lesions: blistering, fragility, pigmentation, erosions
  • associated with Myelodysplasic syndromes

Porphyria cutanea tarda

  • skin lesions: vesicles on sun exposed areas, crusting, superficial scarring, pigmentation
  • PCT-like syndrome can be caused by hexachlorobenezene

Erythropoietic protoporphyria (EPP)

  • skin lesions: NO BLISTERS, photosensitivity, burning, itching oedema after sun exposure
  • associated with myelodysplastic syndromes
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17
Q

Important requirement for urine samples if suspecting acute porphyria

A

Protect from light!

Otherwise, Porphyrinogens oxidised to porphyrins then –> activated porphyrins + O2

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18
Q

Ix results in sick euthyroid

A

o Low T4 (when severe)
o High normal TSH (later becomes low)
o Low T3 and reduced T3 action

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19
Q

Ix results in subclinical hypothyroidism

A

High TSH
Normal free T4

TPO autoantibodies - if positive, can predict future thyroid disease

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20
Q

Ix results in thyrotoxicosis

A
  • Low TSH
  • High free T4, free T3
  • Technetium scan - identify specific cause e.g. single toxic adenoma
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21
Q

Hyperthyroid treatment options

A

Beta blocker (if pulse >100)

Radioactive iodine
- Do NOT use if active thyroid ophthalmopathy

Surgery
- +/- potassium perchlorate before hand to prevent iodide uptake

Thionamides - e.g. Carbimazole, Propylthiouracil

  • Block & replace OR titration regimes
  • NOTE: can cause agranulocytosis - warn pt to stop meds if any sore throat/fever and check FBC!
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22
Q

Vitamin Deficiencies

A

A/retinol - Colour blindness
D/cholecalciferol - Osteomalacia/rickets
E/tocopherol - Anaemia, neuropathy, ?malignany/IHD
K/phytomenadione - Defective clotting

C/ascorbate - Scurvy
Folate - megaloblastic anaemia, NTDs
Niacin - pellagra

Iron - hypo chromic anaemia
Iodine - Goitre, hypothyroidism
Zinc - dermatitis
Copper - anaemia
Fluoride - dental caries
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22
Q

Vitamin Deficiencies

A

A/retinol - Colour blindness
D/cholecalciferol - Osteomalacia/rickets
E/tocopherol - Anaemia, neuropathy, ?malignany/IHD
K/phytomenadione - Defective clotting

C/ascorbate - Scurvy
Folate - megaloblastic anaemia, NTDs
Niacin - pellagra

Iron - hypo chromic anaemia
Iodine - Goitre, hypothyroidism
Zinc - dermatitis
Copper - anaemia
Fluoride - dental caries
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23
Q

Disorders of protein malnutrition

A 
Marasmus
• Shrivelled
• Growth retardation
• Severe muscle wasting
• No subcutaneous fat
Kwashiorkor
• More common at times of famine – carbohydrate remains but protein content reduced
• Scaling/ulcerated
• Lethargic
• Large liver, subcutaneous fat
• Protein deficient
• Oedematous
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24
Q

Causes of SIADH

A
  • CNS pathology – stroke, haemorrhage, tumour
  • Lung pathology – pneumonia (esp Legionella), pneumothorax
  • Drugs – SRRIs, TCA, opiates, PPIs, carbamazepine
  • Tumours
  • Surgery
  • Acute intermittent porphyria
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25
Q

Treatment of hyponatraemia

A

If hypovolaemic: Volume replacement, 0.9% saline

If euvolaemic: Fluid restrict <750ml/day + Abx infusions + Treat underlying cause

  • E.g. hydrocortisone + fludrocortisone in Addison’s
  • E.g. levothyroxine in hypothyroidism
  • E.g. Demeclocycline or Tolvaptan in SIADH

If Hypervolaemic = Fluid restrict <750ml/day + Treat underlying cause + Abx infusions

If severe (reduced GCS, seizures) = hypertonic 3% saline + seek expert help

26
Q

The risk of rapid increase in serum sodium?

A

Central Pontine Myelinolysis

should not increase Na by more than 8-10mmol/L in first 24 hours
Osmotic shifts cause stretching of BBB endothelial cells –> inflammatory signals

Presents with:

  • quadriplegia
  • dysarthria
  • dysphagia
  • seizures, coma, death
27
Q

Management of HYPERnatraemia

A
  1. Fluid replacement – 5% Dextrose
  2. Treat underlying cause
  3. Take serial Na+ measurements every 4-6 hours

If also hypovolaemic, give 0.9% saline to correct ECF depletion (alongside 5% dextrose to correct water deficit)

28
Q

ECG changes in HYPERkalaemia

A
  • Peaked T waves (Early)
  • Broad QRS
  • Flat P-wave
  • Prolonged PR (+ bradycardia)
  • Sine wave (latest)
29
Q

Management of HYPERkalaemia

A

Tx if ECG changes of K+ ?6.5

  • 10ml 10% calcium gluconate
  • 100ml 20% dextrose (previously 50ml 50% dextrose) + 10U insulin
  • Nebulised salbutamol
  • Treat underlying cause
30
Q

Management of HYPOkalaemia

A

If K+ 3.0-3.5
• Oral potassium chloride – 2 x SandoK tablets TDS for 48 hours
• Recheck serum K+

If K+ <3.0
• IV potassium chloride
- Max rate 10mmol/hour
• Rates >20mmol/hour = irritating to peripheral veins

+ Tx underlying cause

31
Q

Management of HYPOkalaemia

A

If K+ 3.0-3.5
• Oral potassium chloride – 2 x SandoK tablets TDS for 48 hours
• Recheck serum K+

If K+ <3.0
• IV potassium chloride
- Max rate 10mmol/hour
- Rates >20mmol/hour = irritating to peripheral veins

+ Tx underlying cause

32
Q

Diagnostic findings in Conn’s syndrome

A

HTN + Low K+

High aldosterone:renin ratio (aldosterone suppresses renin)

33
Q

Normal response to combined pituitary function test

A 
Glucose drops <2mM then recovers
Cortisol reaches 450-550nM (>400)
Growth hormone >10IU/L
LH, FSH, TSH >10IU/L
Prolactin stimulation
34
Q

Treatment of (functioning) prolactinoma

A 
Urgent hydrocortisone
(Fludrocortisone not needed - adrenals make aldosterone independent of hypothalamic-pituitary axis)

Other hormone replacement:

  • levothyroxine
  • oestrogen
  • GH
    • Dopamine agonist e.g., Cabergoline or Bromocriptine to shrink prolactinoma
35
Q

Clinical features of Acromegaly

A
  • Headaches
  • hyperhidrosis
  • Large hands “spade like”
  • Prominent supraorbital ridges
  • Increased interdental spaces
  • Macroglossia
  • Prognathism
  • Bitemporal hemianopia
  • Often presents alongside increased prolactin?
36
Q

Diagnostic Ix for Acromegaly

A

IGF-1 measurement = raised
Oral glucose tolerance test = paradoxical growth hormone rise after glucose given
MRI pituitary = visualise any adenoma

37
Q

Treatment of acromegaly

A 
Trans-sphenoidal surgery (if no lateral growth or involvement of blood vessels)
\+/- Pituitary radiotherapy
D2 receptor agonist e.g. Cabergoline
Somatostatin analogues e.g. Octreotide
GH receptor antagonist e.g. Pegvisomant
38
Q

Osmolality equation

A
  • (Na+, K+) + (Cl-, HCO3-) + Urea + Glucose

* OR just 2 x (Na+, K+) + Urea + Glucose – since do not know anion levels!

39
Q

Anion gap equation

A

Na + K - Cl – HCO3

Normal range = 16-20mM

40
Q

Diagnostic findings in DKA

A

Hyperglycaemia >11.0mmol/L

Ketonaemia >3.0mmol/L OR significant ketonuria (2+ on dip)

Acidosis HCO3- <15.0mmol/L AND/OR venous pH <7.3

41
Q

MOA of diabetes drugs

A

Gliptins e.g., sitagliptin = DPP-4 inhibitors

Thiazolidinediones / glitazones e.g., Pioglitazone = bind to peroxisome proliferator activated receptor-gamma in adipocytes –> maturation of fat cells + reduced circulating fat –> improved insulin sensitivity

Biguanides e.g. metformin = inhibit conversion of lactate to glucose in liver

42
Q

T2DM diagnostic criteria

A

Fasting plasma glucose > 7.0mM OR

Glucose tolerance test (75 grams given at time 0) plasma glucose > 11.1mM at 2 hours OR

HbA1c > 48

NOTE: impaired glucose tolerance is 2-hour value 7.8-11.1mM OR HbA1c >42

43
Q

Summary of adrenal disease

A

Addison’s

  • low Na
  • high K+
  • hypotension
  • Ix = short SynACTHen –> low cortisol
  • Tx = corticosteroid replacement

Phaeo

  • HTN
  • Ix: urine + serum metanephrines (catecholamines, normetanephrines)
  • Tx = alpha blockade, beta blockade, surgery

Conn’s

  • high Na
  • low K
  • HTN
  • Ix: HIGH aldosterone: renin ratio
  • Tx: adrenalectomy OR aldosterone antagonist

Cushing’s

  • centripetal obesity, inter scapular fat pad, bruising etc.
  • DM, HTN
  • low K
  • Ix:
    - - 9am + 12am plasma cortisol –> HIGH
    - - low dose dexamethasone suppression test –> not suppressed
    - - IPSS (pituitary sampling) to identify cause
  • Tx: Treat cause e.g. stop steroids, remove tumour
44
Q

Normal GFR

A

120mL/min

45
Q

Diagnostic criteria for AKI

A
  • Increase in serum creatinine by >26mmol/L within 48 hours OR
  • Increase in serum creatinine to 1.5x baseline within 7 days OR
  • Urine output <0.5ml/kg/hour for 6 hours
46
Q

Stages of AKI

A

Stage 1

  • Increase in serum Cr by ≥26 micromol/L OR by 1.5 to 1.9x the ref serum Cr
  • UO <0.5ml/kg/hour for 6-12 hours

Stage 2

  • Increase in serum Cr by 2-2.9x ref serum Cr
  • URO <0.5ml/kg/hour for ≥12 hours

Stage 3

  • Increase in serum Cr by ≥354micromol/L OR ≥3x ref serum Cr
  • UO <0.3ml/kg/hour for ≥24 hours OR anuria for ≥12 hours
47
Q

Pre-renal causes of AKI

A

Generalised reduction in tissue perfusion or selective renal ischaemia
+ failure of adaptive mechanisms to maintain renal percussion

  • true volume depletion
  • hypotension
  • oedematous states
  • selective renal ischaemia
  • drugs affecting glomerular blood flow - NSAIDs, calcineurin inhibitors, ACEi, ARB, diuretics
48
Q

Renal causes of AKI

A

Abnormality of any part of nephron

• Vascular disease – vasculitis
• Glomerular disease – glomerulonephritis
• Tubular disease – acute tubular necrosis (most common!) from
untreated pre-renal AKI or endogenous/exogenous toxins
• Interstitial disease – analgesic nephropathy

49
Q

Post-renal causes of AKI

A

Physical obstruction to urine flow

  • Intra-renal obstruction
  • Ureteric obstruction – bilateral
  • Prostatic/urethral obstruction
  • Blocked urinary catheter
50
Q

Indications for emergency dialysis in AKI

A
  • (Metabolic) acidosis
  • Refractory hyperkalaemia
  • Lithium, aspirin ‘intoxication’
  • Pulmonary oedema
  • Uraemic encephalopathy, pericarditis
51
Q

Definition/Criteria for Chronic kidney disease

A

Abnormalities of kidney function ≥ 3 months with implications for health

Longstanding decline in GFR (<60) OR 1 of:
• Albuminuria / proteinuria
• Urine sediment abnormalities e.g., haematuria
• Electrolyte abnormalities
• Histological abnormality
• Structural abnormalities (on imaging)
• Hx kidney transplant

52
Q

Stages of CKD

A

G1: GFR >90 with evidence of kidney damage

G2: GFR 60-89

G3a: GFR 45-59
G3b: GFR 30-44

G4: GFR 15-29

G5: GFR <15

53
Q

Most common causes of CKD

A
  • Diabetes!!
  • Atherosclerotic renal disease
  • HTN
  • Chronic glomerulonephritis
  • Infective or Obstructive nephropathy
  • Polycystic kidney disease
54
Q

Progression of Uraemic cardiomyopathy (in CKD)

A

LV hypertrophy
LV dilatation
LV dysfunction

55
Q

Indications for dialysis in CKD

A 
o	Intractable hyperkalaemia
o	Acidosis
o	Uraemic Sx – nausea, pruritis, malaise
o	Therapy-resistant fluid overload
o	CKD Grade 5
56
Q

Patterns of LFT abnormalities

A

High ALP + GGT (ALP&raquo_space;) = biliary obstruction e.g. gallstones, HOP ca.

GGT > ALP = recent ETOH intake

ALP > GGT = pregnancy? osteomalacia (if PTH high), Paget’s disease (if osteocalcin high)

AST + ALT high = hepatocyte damage

  • AST rises most (>ALT) = alcoholic hepatitis / cirrhosis
  • ALT rises most (>AST) = viral hepatitis
57
Q

Tumour markers

A

Ca125 = ovarian

Ca19-9 = pancreatic, cholangiocarcinoma

acid phosphatase / PSA = prostate

CEA = colorectal

AFP = testicular ca. (teratoma), hepatocellular ca.

58
Q

Treatment of acute gout

A

NSAIDs

colchicine - inhibits polymerisation of tubular –> less neutrophil motility –> less inflammation

Glucocorticoids - oral or intra-articular injection

Do NOT attempt to alter plasma urate concentration - can cause further precipitation of crystals!

59
Q

Microscopy of crystal arthropathies

A

Gout (monosodium urate)

  • negative birefringence (yellow when parallel to compensator, blue when perpendicular)
  • needle shaped

Pseudogout (calcium pyrophosphate)

  • weak positive birefringence (blue when parallel to compensator)
  • rod or Rhomboid shaped
60
Q

Pathophysioloy & key features of Lesch Nyhan syndrome

A

X linked
Complete deficiency of H(G)RPT enzyme
No recycling of hypoxanthine or guanine to IMP/GMP

Normal at birth BUT then

  • developmental delay, mental retardation
  • spasticity
  • hyperuricaemia
  • choreiform movements ~1 year
  • self mutilation, aged 1-16yrs (affects 85%)
61
Q

Pathways of purine synthesis

A

De novo

  • metabolically difficult
  • inefficient

Salvage

  • recycles purine catabolites
  • predominates in most tissues EXCEPT bone marrow
  • highly efficient
62
Q

Rate limiting step of Purine Metabolism

A

PAT

  • Negatively regulated by AMP & GMP (end products of purine synthesis)
  • Also subject to positive feed-forward effect by PPRP
63
Q

Transport of thyroid hormone

A

75% thyroid binding globulin

20% TBPA

5% Albumin

0.03% free T4

Path 2022 (12 decks)

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