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Chempathology Flashcards

1
Q

What are the management options for acute hypoglycaemia

A 
Alter & orientated
- carbs
-Rapid= juice/ sweets
-long-acting - sandwich
Drowsy/ confused
-Buccal glucose, hypo stop/ glucogel. Consider IV access
Unconscious/ unsafe swallow 
-IV 50ml, 50% glucose mini-jet or 100ml 20%

IM glucagon Img ( deteriorating, refractory, insulin-induced, difficult IV

All should be monitored

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2
Q

What glucose range is hypoglycaemia

A

<3.5 mmol

Worried <3mmol/L
On ward <4mmol/L
Neonates <2.5mmol/L
(normal is 4-6mmol, can drop lower,3-3.5 following exercise or excessive carbohydrates)
\+ symptoms
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3
Q

What are the symptoms of hypoglycaemia

A

Early Adrenergic: tremors, palpitation, sweating, hunger.
(may not occur in insulin-treated diabetics who are chronically hypo)
Neuroglycopenic: confusion, seizures, coma, death

Should resolve with glucose

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4
Q

What is the order of physiological changes during hypoglycaemia

A
  1. insulin suppression
  2. # Increase glucagonv peripheral glucose uptake
    ^glycogenolysis
    ^gluconeogenesis
    ^lipolysis -> ^free fatty acids (beta-ox ->^ ATP and ketones)
  3. Adrenaline (=slight insulin resistance)
  4. ACTH, cortisol and growth hormone.
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5
Q

What are the investigation confirms hypoglycaemia

A

Confirm hypoglycaemia

  • bm (easy in diabetes, but is inaccurate due to poor precision in normal adults)
  • lab (grey top -fluride oxalate- 2mls blood -gold standard)
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6
Q

What are the causes of hypoglycaemia (without diabetes) (6)

A

Fasting vs reactive
Critical illness, organ failure- liver and renal (no gluconeogenesis), hyperinsulinism, post gastric bypass, drugs, extreme weight loss - eg anorexia, factious

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7
Q

What are the causes of hypoglycaemia in diabetes (5)

A

Hypo unawareness (can be caused by autonomic neuropathy)
Excess insulin or sulphonylureas
Excess EthoH (decreased awareness and ^ glucose)
Strenuous exercise
coexisting AI (additions due to lack of steroids)

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8
Q

What medications can cause hypoglycaemia in diabetes

4 diabetes) (3 other

A

That can cause hypos:
Sulphonylureas and insulin- rapid and long actin.
-Meglitinides, GLP-1
-beta-blockers, salicylate, alcohol

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9
Q

What investigations should be done for hypoglycaemia (non-diabetes)

A

Must be done during the hypo
-Full Hx and Ex
-Need to consider IV access and treatment vs tests
- Bloods: Glucose, Insulin, C-peptide, drug screen , Auto-antibodies, cortisol, GH
FFA, ketones
specialist IGFBP, IGF-2, carnities

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10
Q

Why is measuring c-peptide useful

A

As it is the cleavage product of pro-insulin, it is secreted in equimolar amounts to insulin but has a long T1/2 (30 mins) compared to insulin (minutes)
It can help to determine if insulin is exogenous or endogenous. (c-peptide would be low if exogenous insulin)

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11
Q

How can anorexia cause hypoglycaemia

A

Chronically poor dietary intake can cause depletion of liver glycogen stores
+ acute lack of glucose intake

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12
Q

What can cause hyperinsulinaemic hypoglycaemia?

A

Fasting, critical illness, Anorexia, strenuous exercise, endocrine deficiencies (eg v hypo pit or hypoadrenalism)
Failure- liver, anorexia Nervosa

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13
Q

What are the causes of neonatal hypoglycaemia

A

appropriate (and will improve with feeding)
-Prem, IUGR, small for gestational age, inadequate glycogen and fat stored.
pathological
-inborn errors of metabolism

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14
Q

What are the investigation finding in inborn errors (give examples) of metabolism (neonatal hypoglycaemia)

A

^FFA, no ketone bodies
-Fatty acid oxidation disorder - no ketone production
- Glycogen storage disease T1- gluconeogenic disorder
-Medium-chain acyl-CoA dehydrogenase (MCAD)
Carnitine disorders

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15
Q

What metabolic disorders are screened for on the Guthrie blood spot test ( and their pathology)? (9)

A

Phenylketonuria (phenylalanine hydroxylase v- check levels)
SCD,
MCAD, maple syrup urine disease (MSUD), isovaleric acidaemia, homocystenuria, glutamic acid type 1,
SCID
CF (CFTR gene mutation, immune reactive trypsin+), Congenital hypothyroidism (dys/agenesis of the thyroid gland -TSHv)

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16
Q

Define specificity and sensitivity, PPV / NPV

A

Specificity= Total Negative (False positive+Total negative)
-that someone without the disease will correctly test negative

Sensitivity= Total positive/ (Total positive+ False negative)
- the probability that someone with the disease will test positive

Positive predictive value= Total positive/ (Total positive+False positive)
Negative predictive value = Total negative/ (Total negative +False negative)

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17
Q

What are the different types of metabolic conditions

A 
Accumulation of toxins
Poor energy stores
Large molecule synthesis
errors in large molecule metabolism
Mitochondrial
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18
Q

What metabolic conditions are classified as the accumulation of toxins (3-groups)

A

Organic acidaemia eg propionic (Ketosis, metabolic acidosis, acidaemia
Urea cycle disorders - eg ornithine transcarbamylase v
Amnioacidopathies- PKU, maple syrup urine disease

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19
Q

Which metabolic disorders are caused by defects in large molecule metabolism?

A

Lysosomal disorder eg Tay Sachs disease

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20
Q

What are the general symptoms of hypocalcaemia

A

bone disease, muscle and nerve hyperexcitability

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21
Q

What are the symptoms of hypercalcaemia

A

Bones- boney pain, Stones- renal caulculi, Groans- constipations and Moans - confusion >3mmol/l, seizures coma, Polyuria and poldipsia, osmotic diuretic

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22
Q

What is the function of PTH

A

PTH - increases serum calcium (neutral effect on Pi)
Bones -^ Ca and Pi release - ^osteoblast activation -> ^ proliferation, ^RANK L expression, v OGT expression (this prevents interference with RANK L) -> ^ osteoclast activity
^ Calcitonin - ^ bones and ^ GI
Direct ^ Ca absorption in GI, (indirect via calcitonin for Pi
Kidneys - ^ 1a hydroxylase > ^ active vitamin D, ^ Ca reabsorption, ^ excretion of Pi

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23
Q

How is active vitamin D formed

A

Cholecalciferol
Ergocalciferol - dietary
transformed in the liver to 25,OH D3
1 alph hydroxylase in kidneys -> 1,25 diOH D3

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24
Q

What is the role of vitamin D

A

^ GI absorption of ca and Pi, affects cell proliferation and immunity

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25
Q

Which bone disease have

a. normal calcium
b. low calcium
c. high calcium

A

a. Paget’s - just abnormal structure, Osteoporosis - everything is normal except BMD
b. v Vit D - osteomalacia, ricket’s, renal osetodystrophy -v reasorption and v vit D, pseudohyperparathyroidism, hypoparathyroidism
c. 1 ^PTH, cancer, thiazides, sarcoidosis

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26
Q

Which bone disorders result in an elevated ALP?

A

Paget’s, Vit D deficiency

^/- Primary and secondary PTH++

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27
Q

What is the normal range of sodium?

A

135-145mmol/L

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28
Q

What are some causes of hyponatraemia (volume split)

A

Hypovolaemic - Fluid loss, GI- D&V, renal- salt loosing nephropahty
Euvolaemic- Hypothyroidism, adrenal failure, SIADH
Hypervolaemic - HF, cirrhosis, renal failure

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29
Q

What are some causes of SIADH

A

Respiratory - infection- pneumonia, aspergillosis, abscess, TB
Malignancy- lung small cell or mesothelioma, Gi- stomach, duodenum, pancrease.
CNS- SOC - cancer, bleed, stoke, GBS, MS,
Drug induced- SSRIs, TCA, antipsychotics, MDMA, desmo/vassopressin, oxytocin, opiates
Other- any nause and vomiting, pain, stress, hereditary

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30
Q

What are the investigations for hyponatraemia?

Volume split

A

Assess fluid status - clinical exam and full obs

Hypovolaemic- FBCs, CRP, U&Es- eGFR
Euvolaemic - TFT, short synthactin test, urine and plasma osmolality
Hypervolaemic- ECG/echo, LFTs, U&Es and eGFR

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31
Q

What are the investigations for hypernatraemia

A

bloods - glucose (rule out DM), K+, Ca+ (rule out nephrosis), plasma and urine osmolality

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32
Q

What is the management of hyponatraemia (split by fluid)

A

Hypovolemic- normal saline
Euvolaemic - fluid restriction - if very deficient consult a specialist for initiating 3% saline - do not increase by >8-10% in first 24hrs, <10 after that.
Hypervolaemic - fluid restriction <750ml/ day including abx drip
Always treat underlying cause

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33
Q

What is the management of hypernatraemia?

A

5% dextrose

If hypovolaemic 0.9% normal saline followed by 5% dextrose.

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34
Q

What are the diagnostic criteria for SIADH

A

Euvolaemic hyponatraemia
with normal TFTs and adrenal function
low serum and increased >100 urine osmolality

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35
Q

What is the normal range of plasma potassium?

A

3.5-4.5mmol/L

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36
Q 
What is the effect of 
a. aldosterone
b. insulin
c. beta-agonists
d. loop diuretics
e. spironalcatone
on plasma potassium
A

a. v (via increased excretion of K+ in CD down an electrochemical gradient to compensate for water and Na+ reabsorption.
b. v (Increased uptake into cells)
c. v (also ^ uptake to cells)
d. v (triple transporter inhibition> v K+ reabsorption)
e. ^ - anti-aldosterone

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37
Q

What are the causes of hyperkalaemia?

A

Renal dysfunction - diabetic nephropathy, NSAIDs
v Aldosterone: Addison disease and malignancy
^ release from cells: Acidosis, Rhabdomyolysis
Drug-induced - ACEi, ARBs, spironolactone

ps - consider a haemolysed sample

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38
Q

What is the treatment of hyperkalemia?

A 
>6.5 and or ECG changes
10ml 10% calcium glucontae
50ml 50% dextrose + 10 U insulin
Nebulised salbutamol
<6.5 and no ECG changes - treat cause
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39
Q

What are the causes of hypokalaemia?

A

GI loss - D and V
Renal - ^ aldosterone/ ecess cortisol
^ Na+ reaching DCT - eg loop diuretics, thiazides (nieche batter syndrome, Gitleman, v magnesium, renal tubular acidosis T1 and 2)
osmotic diuresis - eg DM

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40
Q

What is the treatment of hypokalaemia

A

3-3.5 oral KCL TDS 48hrs

< 3 IV KCL max 10mmol/L/Hr ( peripheral vein irritation)

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41
Q

What are the clinical finding of hyperkaelmia? (Ecg)

A

ECG- peaked t waves, flattened p waves, prolonger PR interval, bradycardia

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42
Q

What are the clinical signs and symptoms of hypokalaemia

A

Cardiac arrhythmias, muscle weakness, poluria and polydipsia

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43
Q

What are the buffering methods for pH?

A

^ Renal excretion of H+ > ^ regeneration of bicarb -. mop up H+
^ respiration rate to blow off CO2 > shifts equation to replace CO2 + v CO2

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44
Q

What are the VBG finding of
a metabolic acidosis
b. with compensation

A

a. acidotic <7.35, normal PCO2(4.7-6.0), normal PO2 (10-13), vHCO3 (<22) (if normal consider other acids eg lactate, ketones)
b. v or normal pH, vPCO2, normal PO2, vHCO3

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45
Q

What are the VBG findings of

a. respiratory acidosis
b. with compensation

A

a. ph <7.35, pCO2 >4.7, pO2 - variable - depending if on oxygen and severity, HCO3 normal 22-30

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46
Q

What are the causes of respiratory acidosis?

A

v lung perfusion - PE, RHF
V/Q mismatch
v gas exchange - emphysema

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47
Q

What are the causes of metabolic acidosis?

A

^anion gap MUDPILES
Methanol, Uraemia DKA Propylene glycol Iron tablets Lactic acid Ethelene glycol Salicylates

normal anion gap 6-12 HARDASS
Hyperpigmentations Addison’s Renal tubular necrosis Diahorrea Acetocolamide Spironolactone (^K+) Saline

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48
Q

What are the causes and findings for metabolic alkalosis?

A

pH >7.46, pCO2 normal( 4.7-6.0), pO2 (10-13) normal, HCO3 >22
Compensated - pH v/-, PCO2^, pO2 -, HCO3 >22

Causes: Bicarb intake - antacids, H+ loss- vomiting, Hypokaleamia

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49
Q

What are the causes and findings of respiratory alkalosis?

A

pH >7.46, PCO2 <4.5, PO2, HCO3 -
compensated pH ^/-, PCO2 <4.5, HCO3v

causes: hyperventilation - panic attack, drugs, artificial ventilation

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50
Q

Why is respiratory compensation for metabolic alkolosis limited?

A

^PCO2 will stimulate the respiratory drive to increase resp rate.

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51
Q

What is the equation for osmolality

A

=*2(Na+K+)+ urea + glucose

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52
Q

How is the anion gap calculated?

A

= Na+ K+ - (Cl- and HCO3-)

53
Q

What do the liver function tests look at?

A

AST- liver, (muscle kidney, brain, pancreas)
ALT- liver (muscle, kidney brain pancreas)
ALP - Gallbladder (also bone) (SI, kidney, WBC, placenta)
GGT- gallbladder, chronic alcohol intake (kidney, pancreas, spleen heart, brain, seminial vesicles, liver)
Bilirubin- pre- haemolysis, intra- liver function, post- obstruction
Albumin- chronic synthetic function (T1/2= 20 days)
PT- acute synthetic function
aFP- HCC, pregnancy, prostate cancer

54
Q

What are the functions of the liver

A

intrametabolic- GNG, glycogenolysis, lipid met, FA synth
protein synthesis
xenobiotics- p450, redox, conjugation, excretion
Hormone met
Bile synthesis
Reticulo-endotheliasl- epo and kuffer cells

55
Q

When is it important to look at AST and ALT together

A

AST:ALT ratio >2 indicates alcoholic hepatitis.

>1 but no alcohol history indicated severe cirrhosis-> need further imaging

56
Q

How should you interpret a raised bilirubin?

A

If AST and ALT are raised - intraheptaic causes
If GGT or ALP are raise- cholestatic - USS - dilated - obstruction, undilated- drugs, PSC, PBC

neither - blood film for haemolysis or gilbert

57
Q

What tests are on a liver screen (aka what to do after abnormal lfts)

A 
HBV and HCV
Fasting lipids and glucose
Ferritin and iron studies
coeliac
haemosiderin
Ceruloplasmin <50 Wilson's->urinary copper
Auto antibodies- ASMA, AMA,ANCA
ALpha-1antitrypsin -> phenoptype
Imaging
USS
CT
MRCP
Endoscopic US
58
Q

Which zone of the liver is most susceptible to hypoxia and why

A

Zone 3 as it has the highest metabolic rate and is furtherest form the afferent blood supply

59
Q

What are the histology finding of acute hepatitis?

A

Fatty depositis, megamitochondria
-Mallory hyaline (stains pink) lines -> ballooning which is irreversible damage.
Cirrhosis forms small nodules

60
Q

What is the treatment of alcoholic hepatitis?

A

Stop drinking
Parinex
Steroids - contentious

61
Q

What is the treatment of portal hypertension?`

A

Beta blockers
Sclerotherapy for anastomes
Terlipressin for active bleeding

62
Q

What is the normal histology of the liver?

A

portal triad contains portal vein, hepatic artery and bile ducts. Hepatocytes are organised in trabeculae with central sinusoids that surround a central vein

63
Q

What anastomes get engorged in portal HTN

A 
Oesophageal
Umbilical
Anal
Retroperitoneal
bare area of liver
Patent ductus venosus - rare
64
Q

What are the definitive features of liver failure

A

Failed synthetic function - eg ^INR/PT, v albumin
^ amnion -. encephalopy
Failed clearance of bilirubin

65
Q

Which hormones are released from the pituitary?

A

Anterior - ACTH, GH, LH and FSH, TSH prolactin

Posterior - vasopressin and oxytocin

66
Q

What is the cause of SHeehan’s syndrome?

A

MOH - leads to ischamia of the pituitary gland - which increases in pregnancy.
Characterised by failure to breast feed, amenhorrea and tiredness

67
Q

What are the indications for a pituitary function test

A

Gynaecomastia and amenhorea

68
Q

WHat are the causes of a raised prolactin?

A

> 6000 = prolactinoma
Disconnected hyprolactinaemia =non-functioning pituitary adenoma - causes compression of the stalk > v dopamin > ^ prolactin
Pregnancy
Hypothyroidism (^TRH > ^prolactin

69
Q

How is the triple pituitary stress test done?

A

Fatsed overnight
Given TRH, LHRH and insulin
- measure glucose, TSH, GH, Lh and FSH and basal thyroxine every 30 mins.
Can be dangerous so need ECG and IV access prior- to give dex

70
Q

What are the investigations for acromegaly?

A

OGTT- should suppress GH

IGF-1 and exercise tests

71
Q

What are the investigations for suspected GH deficiency in children

A

Random GH
Exercise tolerance test
Insulin stress test - not first line as dangerous

72
Q

What is the order of importance for pituitary hormone replacement?

A

Cortisol (hydrocortisone)> Thyroxine>oestrogen> growth hormone

73
Q

Describe the synthesis of T3 and T4

A

TRH->TSH-> thyroid.
Uptake of iodide via -Na+/I- symporter- bl mem.
I- -> folliclular space via CL-/I- antiporter on apical mem
TPO oxidises I- ->I
Iodinisation of thyroglublin -> MIT or DIT
MIT + DIT = T3
DIT x2= T4
Stores in lysosome
Released directly into blood stream

74
Q

What are the signs and symptoms of Hypothyroidism?

A

Bradycardia, weight gain, poor appetite, cold intolerance, constipation, low mood, oligo/amenorrhea -> infertility, fatigue, laboured breathing, hyponatraemia, normocytic anaemia, myoedmea, goitre

75
Q

What are the causes of hypothyroidism

A

Hashimoto’s, post-viral thyroiditis, congenital/ acquired, thyroidectomy/ radio, drugs- amiodarone and lithium
Dysgenesis/agenesis
Pituitary dysfunction
Thyroid hormone resistance

76
Q

WHat are the investigations for hypothyroidism

A

TSH, T3, T4, AI screen, ECG

77
Q

What are the signs and symptoms of hyperthyroidism?

A

Tachycardia, sob, diarrhoea, oligomenorrhea, palpitations, AF, sweating, anxiety, increased appetite, ^ energy , osteopenia
(Grave’s- exopthalmos, pretibial myxoedma goitre, thyroid acropatchy (fat fingers)

78
Q

What are the causes of hyperthyroidism?

A

High uptake: Grave’s disease, toxic nodular, single toxic nodule

Low uptake: thyroid cancer, silent thyroiditis- immune and amiodarone, TSHoma, viral thyroiditis, factitious, trophoblastic stumour, struma ovarii

79
Q

What are the investigations for Hyperthyroidism?

A

TSH, T3, technetium uptake scan, AI screen, dexa

80
Q

How is thyroxine affected by pregnancy?

A

Beta HCG stimulates T4 synthesis-> v TSH.
Also ^ TBG due to ^oestrogen= maintained fT4

3rd trimester -> HCG v-> ^TSH

81
Q

What thyroid dysfunction is screen for in neonates?

A

Congenital hypothoroidism on the Guthrie test
48-72hrs
(earlier= maternal, >5 days later = too late to prevent neurodisability)

82
Q

What is sick euthyroid?

A

Severe (non-thyroid) illness eg sepsis -> vfT3 and action, compensatory ^TSH and normal T4

  • does not have clinical signs of hypothyroidism and does not respond to levo
83
Q

What are the different types of thyroid cancer?

A

Medullary- sporadic or MEN2- markers= calcitonin and CEA, Papillary
Treatment is surgical resection or thiamides (cabergoline)- TG = marker of relapse

84
Q

What is functionality of measuring enzymes?

A

Localised damage - leaky membrane -> release of cytosolic enzymes
Necrosis -> intra-organelle enzymes
Local- cell damage- synthesis
Response to treatment
Marker for substrate- eg glucose oxidase for glucose

85
Q

What causes raised ALP and how can you differentiate?

A

> x5 - Paget’s disease, osteomalacia, 1 and 2 ^PTH, Cirrhosis, cholestasis

86
Q

Describe the biomarker tests for myocarial infarction?

A

Myoglobin (non specific)
troponin- being to rais from hrs 4-6, peak at 12-24 and slowly decline over 3-10 days
MB- CK- rapid increase and decrease

87
Q

What can cause a raised amylase?

A

> x10 Pancreatitis- (check lipase as more specific)
any acute abdomen
Salivary form- mumps and parotitis

88
Q

What are the signs and symptoms of Addison’s

A

Significantly worse during acute stress - eg illness, surgery
Weak, dizzy, fatigue, anorexia, muscle or joint pain, D&V, back pain, abdominal pain, hypotension, hyperpigmentation

89
Q

What are the features and treatment of a phaeo

A

Acute hypertension, aggression

Treat with alpha, beta, surgical removal

90
Q

Which hormones are produced in the adrenal glands

A

Adrenal medulla- catecholamines Noradrenaline and adrenaline
Cortex
Zona glomerulosa- mineralcorticoids- aldosterone
Zona fasiculata - glucocorticoids cortisol
Zona reticularis- androgens

91
Q

What is the test for addison’s disease?

A

Short synthactin test - measure cortisol, give synthetic ACTH measure cortisol at 30 and 60 mins

92
Q

What is the test for Conn’s

A

Aldosterone and renin levels and CT

93
Q

What is the tests for Cushing’s

A

9am and midnight cortisol
Dexamethasone suppression test
pituitary sampling
MRI >5mm

94
Q

What is the function of cortisol?

A 
Opposite effect of insulin
^glycogenolysis
^lipolysis
^aminoacid breakdown
^osteoclast activity
^BP and HR
95
Q

What are the requirements for a metobolite clearance = GFR

A

Freely filtered
not protein bound
not resorbed or excreted by tubular cells

96
Q

What are the clinical markers of GFR

A

99Tc DTPA
51 Cr EDTA
creatinine
cystatin C

97
Q

Why is creatinine not an accurate GFR

A

Proportional to muscle mass and injury
v with age
affected by ethnicity
Also variable renal excretion 30-60%

98
Q

What are the different imaging types for kidneys

A

Renal USS - stones with hydronephrosis, AKI- kidney size
CTKUB - first line for stones
Histology
IV urogram - old

99
Q

What is the definition of AKI?

A

Rapid declined in kidney function within hours resulting in an inability to maintain homeostasis in electrolytes, fluids or acid-base

100
Q

What are the different types and aetiologies of AKI

A

pre renal - systemic v blood supple- hypovolemia, hypotension, 3rd spacing, renal specific (RAS), Drugs - ACEi, NSAIDs, calcineurin inhibitors, diuretics

Intra renal - heterogenous

Post renal - obstructive, renal, ureteric, prostatic (BPH, prostatitis and C), extrinsic- catheter > urinary retention

101
Q

What are the classes of AKI

A

Class 1 Serial serum creatinine >26umol 1.5-1.9x normal
Class 2 SSc 2-2.9x normal
Class 3 SSc 3+x normal or 354umol/L

102
Q

What are the consequences of CKD

A

Anamia of chronic disease- v EPO
CVD - vascular calficiation and uraemic cardiomyopathy
Uraemia
Hyperkalaemia- worsened by ACEi and spironalactone
Renal acidosis - v H+ excretion

103
Q

What are the different types of renal bone disease

A

Osteitis fibrosa- ^ osteclast activity - replaced with fibrosis
Osteomalacia- v Vit D
Adynamic bone disease- vpth
Mixed osteodystrophy -^ 2nd and 3rd ^pth

104
Q

What is the treatment of chronic kidney disease

A

Haemodialysis
Peritoneal dialysis
Transplant
Optimise HTN, lipids, DM

105
Q

What are the causes of CKD (9)

A 
DM - most common
HTN
ATN
Atherosclerosis > RAS
Drugs 
Infective/ obstructive - bph
Poly cystic kidneys
Chronic glomerulonephrtisi
106
Q

What is the difference between AKI and ATN

A

AKI is reversible damage that once renal blood flow is correct resolves v GFR

ATN is prolonged ischaemia > damage to tubular cells> irreversible

107
Q

What are the interstial causes of AKI

A

Intrarenal- vasculitis, direct tubular injury- drugs, sepsis contrast dye, toxins - endogenous - myoglobin
exogenous- aminoglycosides, amphotericin and aciclovir
Glomerulonephritis and vasculitis
Abnormal protein deposition- amyloid, MM related, lymphoma

108
Q

What are the criteria required of a screening program?

A 
Important health issue
Ability to be diagnosed
Can be treated
Test suitable and acceptable to public
Scientific understanding of disease progression
Latent/ early symptomatic stage
Economically balanced
Agreed population that require treatment
109
Q

Which disorders are screened for on the Guthrie?

A

Congenital hypothyroidism
severe combined immunodeficiency
CF
SCD

Phenylkenouria
Maple syrup urine disease
Homocysteine uria
Isovaleric acidaemia
Glutaric aciduria T1
MCAD
110
Q

Define

a. sensitivity
b. specificity
c. positive predictive valvue
d. negative predicitive value

A

a. Ability to correctly identify positive cases = Ture+/total with disease
b. Ability to correctly exclude negatives= T-/ total without disease
c. PPV = True + / total +
d. NPV = true -/ total -

111
Q

What are the general things diagnostic tests for metabolic disorder can look for?

A

Deficiency in enzyme >
Excess substrate
Deficiency in product
Abnormal metabolites (as when the substrate is in excess may be processed by alternative enzymes)

112
Q

Describe the pathology and treatment of PKU

A

Phenylalanine hydroxylase deficiency> build-up of phenylalanine (essential amino acid) but CNS toxic > Ig <50
From <6 weeks limit intake but not completely

113
Q

Describe the testing for CF

A

Blood spot -if IRT >99.5 centile (on 3 blood spots) - Test for 4 most common CFR mutations
2+ = CF
1 mutation > expand mutations to 28 most common
0 mutation > repeat IFT in 21-28 days

114
Q

How does MCAD present and how can it be prevented?

A

Neonatal hypoglycaemia and - cot death

Pt has an inability to under go beta-oxidation therefore treatment is regular feeding intervals

115
Q

Describe the general presentation of a urea metabolic disorder and treatment?

A 
Hyperammonaemia
Vomiting (no D), respiratory alkosis, encephalopathy, avoidance of protein, coma

labs= ^glutathione, ^/ absent AAs, coma if >300mmol/L ammonia

116
Q

Describe the presentation of a hyperammoniamic organic metabolic acidosis

A

Non lactate metabolic acidosis with a high anion gap
Neonate : funny smelling urine, lethargy, Hypotonic trunk, hypertonic limbs
myoclonic jerks, coma

Older = recurrent ketoacidotic comas and cerebral abnormalities

117
Q

Describe the presentation of reye syndrome

A

Induced by salicylates - eg asprin, antiemetics and valproate
Vomiting, lethargy, confusion, seizure, decerebration, respiratory arrest

118
Q

What is the cause of organic hyperammonia acidosis?

A

Inability to process aminoacids with branched side chains eg leucine, isoleucine, valine
Inability to excrete these> ^ anion gap

119
Q

When should you suspect a mitochondrial disorder and how would you confirm?

A

Multisystem involvement of highly metabolically activity - eg Brain, muscles, kidneys, liver, eyes, endocrine
Lactate^ even after fastine, ^CSF lactate and pyruvate, unexplained ^CK
Muscle biopsy= ragged red fibres
mitochondrial DNA analysis

120
Q

WHat is the pathology of

a. lysosomal storage disorders
b. galactosaemia
c. glycogen storage disease T1 (von Gierke)
d. peroxisomal disorders
e. congenital disorders of glycosylation

A

a. Deficiency in different lyoszymes = heterogeneous presentations > intraorganelle accumulation >organomegaly
b. Inability to breakdown galactose (avoid all dairy) - Glactose-1-phophate uridyl transferase deficiency
c. Inability to dephosphyrlate G1p and G6P > ^glycogen stores > hypoglycaemia
d. Impaired metabolism of VLCFA and phospholipid synthesis
e. In ability to glycosylate proteins

121
Q

What is the role of purines? (3)

A

Guanine, Adenosine (and intermediate inosine)
Genetic code
Secondary messenger cAMP, cGMP
Energy transfer ATP

122
Q

Describe the catabolic pathway of purines? (including excretion)

A

Purines >Hypo xanthine > xathine > (xanthine oxidase)> urate (uritase is non functional in humans)

123
Q

Why does gout typically affect the first MTP?

A

Gout affects the 1st MTP commonly because it is a distal cooler joint so more prone to precipitating out.
Urate circulates at a level close to the limit of solubility, and its solubility decreases at cooler temperatures and lower pHs.

124
Q

What is the rate limiting step of denovo purine synthesis and the feedback it receives?

A

PAT
Negative feedback from adenosine and guanine
Positive feedback from PRPP (substrate and also part of the recycling pathway)

125
Q

Explain the findings on joint effusion for gout and pseudogout?

A

Gout - negatively birefringent needles - appear yellow in the plain of the polariser and blue in the perpendicular plain as it has the ability to bend polarised light
Pseudogout - blocky crystals positively bifingent - blue in the plain and yellow perpendicular

126
Q

What is the acute and chronic management of acute gout (podagra)?

A

Acute - NSAIDs (no if CKD), joint steroid, Colchine

Chronic - ^water intake, reverse any contributing factors, allopurinol (do not give with azathioprine)

127
Q

What is the pathology of lesch Nyhan syndrome

A

XR linked HPRT deficiency

Inability to do salvage pathways > ^ PRPP > ^ PAT activity, vA and G > ^PAT activity

128
Q

What are the s&S of Lesch nyhan syndrome?

A

Well at birth, at 6 months > choriform movements, spasticity, self mutilation severe cognitive impairment, failure to reach milestons

Pathology (6 decks)

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