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flashcards of path guide 2018 > Chem path > Flashcards

Chem path Flashcards

1
Q

feature of hypercalcaemia

A

bone (fractures)
moans (depression)
groans (abdo pain)
stones (kidney stones)

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2
Q

features of hypocalcaemia

A

neuromuscular excitability leading to fits

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3
Q

colle’s fracture

A

posterior displacement of the wrist resulting into a fracture

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4
Q

causes of a colle’s fracture

A

falling onto an extended hand

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5
Q

smith’s fracture

A

anterior displacement of the wrist

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6
Q

causes of a smith’s fracture

A

falling onto a flexed hand

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7
Q

Pott’s fracture

A

fracture of the tibia and fibula

ANKLE FRACTURE

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8
Q

best investigation for suspected renal stones

A

abdo XRAY

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9
Q

first blood test to do when renal stones detected on xray

A

serum calcium

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10
Q

differential diagnosis of a raised calcium

A

1) cancer
2) hyperparathyroidism
3) sarcoid

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11
Q

what does a normal PTH with a high calcium mean

A

PRIMARY HYPERPARATHYROIDISM

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12
Q

how do you differentiate between the three differentials for high calcium

A

differentials (cancer, primary hyperparathyroidism, sarcoid)

test: PTH

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13
Q

how does PTH increase serum calcium

A

increased absorption in the SI
increased release of calcium from bones
reduced calcium excretion in urine

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14
Q

where does 1 alpha hydroxylase act

A

liver

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15
Q

where does 1,25 hydroxylase act

A

kidney

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16
Q

which enzyme does PTH regulate

A

25 hydroxylase

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17
Q

eye sign of hypercalcaemia

A

band keratopathy

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18
Q

complications of hypercalcaemia

A 
osteofibrosis cystica
pepper pot skull
polydipsia
peptic ulcer disease
pancreatitis
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19
Q

how does hypercalcaemia cause polydipsia

A

calcium is an osmotic diuretic

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20
Q

MEN1 complications

A

parathyroid hyperplasia
pituitary adenoma
pancreatic tumours

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21
Q

MEN2 complications

A

parthyroid hyperplasia
pheochromocytoma
medullary thyroid carcinoma

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22
Q

how to treat hypercalcaemia

A

FLUIDS FLUIDS FLUIDS

SALINE

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23
Q

how to cure the hypercalcaemia due to primary hyperparathyroidism

A

parathyroidectomy

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24
Q

what do you give with the IV saline in the treatment of hypercalcaemia

A

frusemide (loop diuretic)

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25
Q

which diuretic must be avoided in hypercalcaemic patients

A

thiazides

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26
Q

why can you normally detect intracellular enzyme in the plasma

A

due to increased cell turnover

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27
Q

what can cause increased plasma enzyme levels

A

tissue injury or cell breakdown

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28
Q

what order are cardiac enzymes released in

A

myoglobin (cytosolic)
CK (nucleus and mitochondria)
troponin (contractile apparatus)

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29
Q

what is special about order of troponin release

A

some troponin is in the cytoplasm and so there is an initial small rise. However most is in the contractile apparatus and is released later causing the sustained late rise

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30
Q

causes of raised enzyme levels

A

increased synthesis

reduced clearance

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31
Q

where is ALP made

A

bone
liver
placenta
intestine

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32
Q

what is an isoenzyme

A

an enzyme that exists in a different form

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33
Q

if someone presents to GP with raised ALP and RUQ pain what else would you check in LFTS

A

GGT

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34
Q

how do you differentiate between liver and bone ALP

A

also measure GGT
electrophoretic seperation
bone specific immunoassay

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35
Q

physiological causes of raised ALP

A

pregnancy

growth spurt in a child

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36
Q

pathological causes of raised ALP (>5x)

A

BONE: paget’s, osteomalacia
LIVER: cholestasis, cirrhosis

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37
Q

pathological causes of raised ALP (<5x)

A

BONE: tumour, infiltration, osteomyelitis
LIVER: hepatitis, infiltrative disease

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38
Q

causes of high serum amylase

A

mumps, pancreatitis, salivary disorders (salivary amylase is an isoform)

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39
Q

risk factors for statin related myopathy

A

polypharmacy
FH
high dose
PMH with a different statin

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40
Q

causes of a raised CK

A 
being afrocarribean
MI (>10x)
Duchenne muscular dystrophy (>10x)
rhabdomyelysis
severe exercise
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41
Q

when are enzymes used to measure therapeutic response

A

Measurement of thiopurine methyltransferase (TPMT) activity is encouraged prior to commencing the treatment of patients with thiopurine drugs such as azathioprine, 6-mercaptopurine and 6-thioguanine

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42
Q

when are enzymes used to measure other substances

A

glucose oxidase as a reagant to measure glucose

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43
Q

diagnostic criteria of an acute MI

A

troponin rise and fall with

a) ischemic symptoms
(b) pathologic Q waves on the ECG
(c) ECG changes indicative of ischemia
(d) coronary artery intervention

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44
Q

what is the unit of enzyme activity

A

U

quantity of enzyme to catalyse 1umol of substrate per minute

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45
Q

what is the ratio of intracellular to extracellular fluid

A

2:1

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46
Q

which has more sodium, intracellular or extracellular fluid

A

extracellular

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47
Q

which has more potassium, intracellular or extracellular fluid

A

intracellular

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48
Q

define osmolarity

A

number of particles in a solution

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49
Q

units of osmolaLity when measured with an osmometer

A

mmol/Kg

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50
Q

units of osmolarity when it is calculated

A

mmol/L

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51
Q

equation for osmolarity

A

2(Na+K)+ urea +glucose

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52
Q

pathological determinants of osmolarity

A

endogenous: glucose
exogenous: mannitol and ethanol

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53
Q

normal range of osmolality

A

275-295mmol/kg

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54
Q

what is the difference between osmolarity and osmolality

A

osmolar gap

if high- metabolic acidosis

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55
Q

what does an osmolar gap mean re metabolic acidosis

A

osmolaRity is lower than osmolaLity

extra unmeasured solutes are dissolved in serum

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56
Q

how is sodium concentration maintained

A

actively pumped from ICF to ECF by Na/K/ATPase

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57
Q

how do you know if someone has true hyponatraemia

A

serum osmolarity is low and sodium is also low

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58
Q

symptoms of hyponatraemia

A

N&V (<136mmol)
confusion <131mmol)
seizures and non-cardiogenic pulm oedema (<125mmol)
coma(<117mmol)

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59
Q

causes of hyponatraemia with a high serum osmolarity

A

mannitol/ glucose infusion

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60
Q

causes of hyponatraemia with a normal serum ofmolarity

A

pseudohyponatraemia (paraproteinaemia or hyperlipidaemia)

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61
Q

causes of hyponatraemia with low serum osmolarity

A

true hyponatraemia

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62
Q

causes of hyponatraemia with hypervolaemia

A

THE FAILURES
heart failure, renal failure and liver failure

FLUID RESTRICT

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63
Q

causes of hyponatraemia with euvolaemia

A

THE ENDOCRINE CAUSES

hypothyroidism, glucocorticoid insufficiency or SIADH

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64
Q

causes of hyponatraemia with hypovolaemia

A

SALT LOSS
D&V
diuretics
salt losing nephropathy

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65
Q

tests in a euvolaemic hyponatraemic patient

A

TFT
short synACTHen test
paired urine
serum osmolarity

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66
Q

treatment of a hypovolaemic hyponatraemic patient

A

restore fluid with 5% dextrose

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67
Q

what determines urine sodium output

A 
RAS
aldosterone
renal function
naturitic peptides (BNP and ANP)
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68
Q

where is aldosterone synthesised

A

zona glomerulosa of the adrenal gland

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69
Q

function of aldosterone

A

sodium reabsorption in kidney and urinary excretion of potassium

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70
Q

how to differentiate between renal and non renal causes of hyponatraemia

A

urinary sodium

20mmol/L is always cutoff

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71
Q

what rate do you correct sodium at and why

A

1mmol/L/hr

risk of central pontine myelinolysis

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72
Q

what is central pontine myelinolysis

A

psuedobulbar palssy, parapariesis, locked in syndrome,

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73
Q

causes of hyponatraemia after surgery

A

over hydration with hypotonic saline

increase ADH release by body as a stress response to surgery

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74
Q

what type of hyponatraemia is SIADH

A

euvolaemic hyponatraemia

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75
Q

is the urine osmolarity high in SIADH

A

YES

lots of water reabsoption

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76
Q

causes of SIADH

A

malignancy:SCLC, pancreas, prostate and lympohoma
chest: TB
CNS: abscess, trauma, meningoecephalitis
drugs: SSRI, carbamezapine, opioids, PPI

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77
Q

treatment of SIADH

A

FLUID RESTRICT

can use tolvaptan and demeclocycline to induce DI (not on NHS)

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78
Q

define hypernatraemia

A

plasma sodium is greater than 148mmol/L

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79
Q

complications of rapid correction of hypernatraemia

A

cerebral oedema

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80
Q

causes of hypovolaemic hypernatraemia

A

water is lost more than sodium
D&V
burns
renal loss: loop diuretics or osmotic diuresis after initial hyponatraemia

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81
Q

causes of euvolaemic hypernatraemia

A

DI
skin (sweating, fever)
resp (tachypnoea)

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82
Q

symptoms of hypernatraemia

A

thirst, confusion, seizures, coma

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83
Q

causes of hypervolaemic hypernatraemia

A 
CONNS syndrome (excess mineralocorticoids)
hypertonic saline
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84
Q

diabetes indipidus

A

HYPERNATRAEMIA (euvolaemia)

no ADH or insensitive to ADH

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85
Q

how to diagnose DI

A

8 hour fluid deprivation test

urine DOES NOT CONCENTRATE

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86
Q

how to differentiate between cranial and nephrogenic DI

A

cranial- urine concentrates with desmopressin administration, nephrogenic stays dilute

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87
Q

primary polydipsia

A

sx of DI but urine concentrates 400-600mosm/kg in fluid deprivation

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88
Q

causes of nephrogenic DI

A

lithium, democlocycline
inherited channelopathy
hypercalcaemia

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89
Q

what is the predominant intracellular cation

A

potassium

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90
Q

causes of hypokalaemia

A

1) GI loss
2) renal loss
3) drugs : Beta blockers, insulin causing redistribution
metabolic alkalosis causing redistribution into cells
4) renal tubular acidosis
5) hypomagnesia

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91
Q

Type 1 renal tubular acidosis

A

failure of hydrogen ion pumping at distal tubule
H+ is not excreted resulting in acidosis and hypokalaemia
SEVERE

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92
Q

Type 2 renal tubual acidosis

A

failure to reabsorb bicarbonate at the proximal tubule resulting in acidosis and hypokalaemia
mild

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93
Q

tybe 4 renal tubular acidosis

A

aldosterone deficiency/ resistance

acidosis with hypERkalaemia

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94
Q

how to treat hypokalaemia

A

sandoK
monito
IV KCl if <3mmol/L but infusion rate of <10mmol/hr to avoid arrthmia

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95
Q

increased intake causing hyperkalaemia

A

fasting
parenteral
stored blood

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96
Q

transcellular movement causing hyperkalaemia

A

acidosis
DKA
rhabdomyelysis

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97
Q

reduced excretion causing hyperkalaemia

A 
acute renal failure
potassium sparing diuretics e.g. spironalactone
ARB
ACEI
NSAIDS
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98
Q

treatment of hyperkalaemia

A 
10%10ml calcium gluconate
100ml 20% dextrose
10 units insulin
salbutamol as an adjunct
TREAT THE CAUSE
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99
Q

causes of metabolic acidosis

A

DKA
renal tubular acidosis
intestinal fistula

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100
Q

causes of metabolic alkalosis

A

pyloric stenosis
hypokalaemia
ingestion of bicarbonate

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101
Q

causes of respiratory acidosis

A

lung injury e.g. pneumonia
COPD
decreased ventilation: morphine OD

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102
Q

causes of respiratory alkalosis

A

mechanical ventilation

panic attack

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103
Q

causes of elated anion gap metabolic acidosis

A

Ketoacidosis
Uraemia
Lactic acidosis
Toxins (ethylene glycol, methanol, paraldehyde, salicylate)

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104
Q

anion gap calculation

A

(Na+K)-(cl+HCO3)

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105
Q

markers for liver function

A

clotting (INR)
albumin
glucose

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106
Q

markers of liver cell damage

A 
ALT
AST
GGT
alk phos
bilirubin
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107
Q

AST:ALT ratio in alcoholic liver disease

A

2:!

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108
Q

AST:ALT ratio in viral liver disease

A

<1:1

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109
Q

when does alk phos rise

A

PREGNANCY

cholestasis

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110
Q

when do you use GGT

A

to confirm raised liver ALP

elevated in chronic alcohol disease, bile duct disease and metastatic disease

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111
Q

define porphyria

A

deficiency of enzyme in the haem synthesis pathway causing overproduction of toxic haem precursors resulting in neurovisceral attacks or cutaneous skin lesions

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112
Q

where is ALA synthase found

A

every cell

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113
Q

what is 5ALA also known as

A

delta ALA

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114
Q

what is PBG synthase also known as

A

ALA dehydratase

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115
Q

how is acute intermittent porphyria inherited

A

autosomal dominant

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116
Q

what is the defect in acute intermittent porphyria

A

HMB synthase deficiency

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117
Q

symptoms of acute intermitten porphyria

A

neurovisceral sx

abdo pain, seizures, psych disturbances, vomiting, tachycardia, sensory loss, hypertension, weakness, constipation

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118
Q

how to diagnose acute intermittent porphyria

A

port wine urine

ALA and PBG in urine

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119
Q

factors inducing AIP attack

A

starvation, premenstrual, stress and ALA synthase inducers e.g. barbiturates, ethanol and steroids

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120
Q

how to treat AIP

A

IV haem arginate
IV carbohydrate
analgesia
avoid precipitants

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121
Q

ALA synthase deficiency

A

NOT A PORPHYRIA

linked with x-linked sideroblastic anaemia

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122
Q

ALA dehydratase deficiency (plumboporphyria)

A

acute neurovisceral
coma, bulbar palsy, abdo pain
build up of ALA

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123
Q

another name for ALAdehydratase

A

PBG synthase

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124
Q

congenital erythropoeitc porphyria enzyme

A

deficiency in uroporphyrinogen III synthase

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125
Q

CEP substance buildup

A

ALA PBG and HMB

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126
Q

CEP symptoms

A

non acute cutaneous lesions

skin blistering and fragility

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127
Q

Porphyria cutanea Tarda (PCT)

A

non acute skin lesions

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128
Q

PCT symptoms

A

vesicles on sun exposed areas with blistering and scarring

raised uroporphyrinogen and ferritin

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129
Q

HCP

A

acute skin
use stool sample
skin blistering in sun exposed areas

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130
Q

Variegate porphyria (VP)

A

protoporphyrinogen deficiency

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131
Q

variegate porphyria pathology

A

build up in protopophyrinogen IX

found in stool

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132
Q

EPP

A

defiency in ferrochelatase
paediatric
non blistering redness minutes after sun exposure

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133
Q

hormones of the anterior pituitary

A 
Prolactin
TSH
GH
LH
FSH
ACTH
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134
Q

symptoms of anterior pituitary failure

A

galactorrea

amenhorrea

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135
Q

what complication is caused by a pituitary macroadenoma and how is it tested

A

bitemporal hemianopia

Humphrey’s 30-2 test

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136
Q

what level of prolactin makes you “almost” certain its a prolactinoma

A

6000

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137
Q

how to investigate a suspected prolactinoma

A

Visual fields
Pituitary function test (stress test)
MRI

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138
Q

What is a pituitary function test

A

induce stress by fasting (hypoglycaemia)
LH
TRH
this should induce ACTH and GH release

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139
Q

in a functioning pituitary what hormones are produced ina pituitary stress test

A

ACTH via CRH

GH via GHRH

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140
Q

what needs to be checked before a pituitary stress test

A

no epilepsy

no cardiac risk factors

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141
Q

how to rescue a hypoglycaemic patient in a pituitary stress test

A

get good IV access

50ml 20% dextrose

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142
Q

what quantities of hormone are given in pituitaty function test (CPFT)

A

200mcg TRH
100mcg LHRH
0.15 units insulin/kg

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143
Q

what needs to be replaced in anterior pituitary failure

A

HYDROCORTISONE
thyroxine
oestrogen
GH

144
Q

how to treat prolactinoma

A

cabergoline

bromocriptine

145
Q

how does a nonfuncitoning adenoma cause hyperprolactinaemia

A

it presses on the stalk so dopaminecan’t reach the pituitary

146
Q

adaquate cortisol response in CPFT

A

Adequate cortisol response = ↑ greater than 170 nmol/l to above 500nmol/l.

147
Q

adaquate GH response in CPFT

A

Adequate GH response = ↑ greater than 6mcg/L

148
Q

adequate TSH response in CPFT

A

> 5mU/L

30 minute response greater than 60 minute

149
Q

normal LH response in CPFT

A

> 10U/L

150
Q

normal FSH response in CPFT

A

> 2U/L

151
Q

reduced TSH

reduced T4

A

central hypothyroidism

hypothalamic/ pituitary failure

152
Q

high TSH

low T4

A

hypothyroidism

153
Q

high TSH

normal T4

A

treated hypothyroidism

subclinical hypothyroidism

154
Q

high TSH

A

TSH secreting tumour

TSH resistance

155
Q

low TSH

high T3, T4

A

hyperthyroidism

156
Q

causes of high uptake hyperthryrodism

A

Graves disease
toxic multinodular goitre
single thyroid adenoma

157
Q

causes of low uptake thyroiditis (hyperthyroidism)

A

De Quervain’s thyroiditis

post partum thyroiditis

158
Q

what is de quervains thyroiditis

A

post viral painful nodule causing hyperthyroidism

159
Q

causes of autoimmune hypothyroidism

A

Hashimoto’s thyroiditis

primary autoimmune hypothyroidism

160
Q

what is hashimoto’s thyroiditis

A

autoimmune disorder post viral antibodies cause initial hyperthyroidism then hypothyroidism.

161
Q

non-autoimmune causes of hypothyroidism

A

iodine deficiency
drug induced- lithium, amiodarone
post RT/ thyroidiectomy

162
Q

treatment of high uptake hyperthyroidism

A

beta blockers

carbimazole

163
Q

treatment of de quervains hyperthroidism

A

NSAIDS

beta blockers

164
Q

types of thyroid cancer

A 
medullary
papilliary
follicular
anaplastic
lymphoma
165
Q

medullary thyroid cancer

A

MEN2a

produces calcitonin

166
Q

how to differentiate pituitary cushings from non-pituitary

A

dexamethasone suppresion test

low dose will fail to suppress pituitary cushings but high dose will

167
Q

how to test for addisons disease

A

synACTHen test

give hydrocortisone unless adrenal lesion when fludrocortisone needs to be given first

168
Q

investigation in conn’s syndrome

A

aldosterone: renin ration

aldosterone is high but renin is low

169
Q

pathology of conn’s syndrome

A 
HYPERALDOSTERONISM
very high BP
resistant to tx
high sodium
low potassium
170
Q

treatment of conn’s syndrome

A

aldosterone antagonists

potassium sparing diuretcis e.g. spironalactone, amiloride

171
Q

how to diagnose a phaeochromocytoma

A

24 hour urinary and plama metadremaline/ catecholamine measurement

172
Q

how to treat a phaeochromocytoma

A

alpha blockade then beta blockade

resect tumour once bp is well controlled

173
Q

phenytoin toxicity

A

ataxia

nystagmus

174
Q

phenytoin under-treatment

A

seizures

175
Q

phenytoin cautions and treatment

A

at high levels liver becomes saturated and so blood levels surge: reduce/ omit doses

176
Q

digoxin toxicity

A

arrythmias
xanthopsia- seeing yellow
confusion
heart block

177
Q

digoxin under-treatment

A

arrythmias

178
Q

cautions with digoxin

A

levels increase if hypokalaemia

caution with renal impairment patients

179
Q

treatment of digoxin toxicity

A

digibind

180
Q

signs of lithium toxicity

A 
lethargy
tremor 
fits
arrythmia
renal failure
181
Q

signs of lithium undertreatment

A

mania

182
Q

cautions with lithium treatment

A

hyponatraemia or decreased renal function/ diuretics cause impaired excretion and levels rise

183
Q

gentacmycin toxicity

A

tinitus
deafness
nystagmus
renal failure

184
Q

theophyline

A

COPD treatment

185
Q

theophyline toxicity

A

arrthmia
tremor
anxiety
convulsions

186
Q

theophyline under-treatment

A

no effect on bronchial smooth muscle

187
Q

cautions in theophyline therapy

A

if erythromycin or phenytoin use levels rise
takes longer for non-smokers liver to clear
if liver failure difficulty clearing

188
Q

causes of primary hypercholestrolaemia

A

type 2 familial hypercholesterolaemia
polygenic hypercholesterolaemia
familial hyperalpha-lipoproteinaemia
phyosterolaemia

189
Q

causes of primary hypertriglyceridaemia

A

type I, V, VI

190
Q

primary mixed hyperlipidaemia

A

familial combined hyperlipidaemia
familial hepatic lipase deficiency
familial dysbetalipoproteinaemia

191
Q

causes of hypolipidaemia

A

AB lipoproteinaemia
hypo alpha lipoproteinaemia
hypobeta lipoproteinaemia
Tangier disease

192
Q

what does PCSK9 do

A

binds LDLR and forces its degradation

193
Q

what happens if PCSK9 is low

A

low LDL levels

194
Q

autosomal dominant mutation in familial hypercholesterolaemia (type 2)

A

PCSK9. apoB, LDLR

195
Q

autosomal recessive causes of type 2 familial hypercholesterolaemia

A

LDLRAP1

196
Q

cause of familial hyperalphalipoproteinaemia

A

CETP deficiency

197
Q

cause of phytosterolaemia

A

ABC G5 and G8

198
Q

cause of type 1 primary hypertriglyceridaemia

A

lipoprotein lipase or apoC II

199
Q

cuase of type 5 primary hypertriglyceridaemia

A

apoA V deficiency

200
Q

cause of type 6 hypertriglyceridaemia

A

increased triglyceride synthesis

201
Q

cause of alphabetalipoproteinaemia

A

MTP deficiency

202
Q

hypoA- lipoproteinaemia

A

apoA-I mutation

203
Q

hypoB lipoproteinaemia

A

apo~B protein is truncated

204
Q

tangier deficiency

A

HDL deficiency

205
Q

lipoprotein order of desity

A 
chylomicron
FFA
VLDL
IDL
LDL
HDL
206
Q

vitamin A excess

A

exfoliative dermatitis

207
Q

vitamin A deficiency

A

colour blindness

208
Q

vitamin A testing

A

in serum

209
Q

vitamin D deficiency

A

osteomalacia/ rickets

210
Q

vitamin D excess

A

hypercalcaemia

211
Q

vitamin D testing serum

A

serum

212
Q

vitamin E name and where found

A

tocopherol and in serum

213
Q

vitamin E deficiency

A

anaemia

neuropathy

214
Q

vitamin K

A

defective clotting

215
Q

vitamin K testing

A

PTT

216
Q

vitamin K name

A

phytomenadione

217
Q

how to test vit B1

A

RBC transketolase

218
Q

vitamin B1

A

Beri Beri
wernicke’s
neuropathy

219
Q

vitamin B2 deficiency

A

glossitis

220
Q

vitamin B2 test

A

RBC glutathione reductase

221
Q

vitamin B6 name

A

pyridoxine

222
Q

vitamin B6 deficiency

A

anaemia

dermatitis

223
Q

vitamin B6 testing

A

RBC AST activation

224
Q

vitamin B6 excess

A

neuropathy

225
Q

vitamin B12 name

A

cobalamine

226
Q

vitamin B12 deficiency

A

`pernicious anaemia

227
Q

how to test vitamin B12

A

serum B12

228
Q

vitamin C name

A

abscorbate

229
Q

vitamin C deficiency

A

scurvy

230
Q

vitamin C excess

A

renal stones

231
Q

vitamin C testing

A

plasma

232
Q

folate deficiency

A

neural tube defects

megaloblastic anaemia

233
Q

how to test folate levels

A

RBC folate

234
Q

vitamin B3 name

A

niacin

235
Q

vitamin B3 deficiency

A

pellagra (dementia, diarrhoea, dermatitis)

236
Q

iron deficiency

A

hypochromic anaemia

237
Q

how to test iron levels

A

ferratin
FBC
Fe

238
Q

iodine deficiency

A

goitre

hypothyroidism

239
Q

zinc deficiency

A

dermatitis

240
Q

copper deficiency

A

anaemia

241
Q

copper excess

A

wilsons

242
Q

copper levels testing

A

cu caeoplasmin

243
Q

flouride deficiency

A

dental caries

244
Q

flouride excess

A

flourosis

245
Q

what is screened for in the gunthrie test

A 
phenylketonuria
medium chain acylcoA dehydrogenase deficiency
congenital hypothyroidism
CF
sickle cell disease
246
Q

what is phenylketonuria

A

phenylanine hydroxylase deficiency

247
Q

how to you screen for phenylketonuria

A

phenylanine levels in blood

248
Q

congenital hypothyroidism pathology

A

dys/agenesis of the thyroid gland

249
Q

Cystic fibrosis pathology

A

CFTR gene mutation

250
Q

screening for congenital hypothyroidism

A

TSH levels

251
Q

how to test for cystic fibrosis

A

immune reactive trypsin is positive

252
Q

how to detect medium chain acyCoA dehydrogenase deficiency

A

acylcarnatine levels by tandem mass spectroscopy

253
Q

specificity

A

those who test negative correctly

Total negative/(false postive +true negative)

254
Q

sensitivity

A

correctly test positive

Total positive/ (false negative + true positive)

255
Q

Positive predictive value

A

the probablitiy test will correctly identify someone with the disease
TP/ (TP+FP)

256
Q

negative predictive value

A

the probability that somebody without the disease tests negative
TN/ (TN+FN)

257
Q

fasting glucose levels to diagnose diabetes

A

> 7

258
Q

random glucose levels to diagnose diabetes

A

> 11.1

259
Q

OGTT levels to diagnose diabetes

A

> 11.1

260
Q

HBA1c levels to diagnose diabetes

A

> 48

261
Q

cause of hyperinsulinaemic hypoglycaemia

A

iatrogenic insulin
sulfonylurea excess
insulinoma

262
Q

cause of hypoinsulinaemic hypoglycaemia with ketones

A 
alcohol binge
no food
liver failure
pituitary insufficiency
addison's
263
Q

cause of hypoinsulinaemic hypoglycaemia with no ketones

A

non pancreatic neoplasms e.g. fibromata or fibrosarcomata

264
Q

non-islet tumour hypoglycaemia

A

low glucose, low insulin, low c eptite, low FFA and low ketones

265
Q

mmeachanism of non-islet cell tumour hypoglycaemia

A

paraneoplastic syndrome

tumouyr secretes big IGF2 which binds to IGF1 and insulin receptors

266
Q

normal GFR

A

120 ml/minute

267
Q

age related GFR decline

A

1ml/hr/yr

268
Q

clearance definition

A

volume of plasma that can be cleared of a marker per unit time

269
Q

conditions for a marker to measure clearance

A

marker cannot bind to serum protein
marker must be freely filtered by glomerulus
marker cannot be secreted/ reabsorped by glomerular cells

270
Q

gold standard measure of GFR

A

inulin

271
Q

endogenous marker of GFR

A

creatinine

272
Q

what to measure in a single sample of urine

A

dipstick
microscopy
protein: creatinine ratio

273
Q

what to measure in 24 hour urine collection

A

stone forming elements
proteinuria quantification
creatinine clearance
electrolytes

274
Q

urine microscopy

A 
test crystal
rbc
wbc
casts
bacteria
275
Q

AKI definition

A

creatinine clearance rising 1.5x baseline in 48 hours or rising over26.5 in 48 hours

276
Q

severe AKI creatinine change

A

3x rise in creatinine clearance

277
Q

pre-renal cause of AKI

A

reduced renal perfusion

hypovolaemia

278
Q

renal cause of AKI

A

vascular, tubal, interstitial or glomerular

279
Q

post renal causes of AKI

A

outflow obstruction

280
Q

indications for emergency dialysis

A 
pulmonary oedema
refractory hyperkalaemia
,metabolic acidosis
uraemic encephalopathy
lithium toxicity
281
Q

common causes of CKD

A 
diabetes
arethosclerotic diseae
hypertensionchronic glomerulonephritis
infective or obstructive uropathy
polycystic kidney disease
282
Q 
consequences of CKD
metabolic
hormonal
CVS
urea
A

metabolic: hyperkalaemia, acidosis
hormonal: reduced epo and anaemia and hyperparathyroidism secondary to low vit D
CVS: vascular calcification and atherosclerosis, uraemic cardiomyopathy
uraemia

283
Q

CKD staging

A

1: GFR>90
2. mild GFR 60-89
3 moderate GFR 30-59
4 severe GFR 15-29
5. ESRF <15 GFR or on dialysis

284
Q

two actions of purines

A

secondary messengers for hormones e.g. cAMP

energy transfer e.g. ATP

285
Q

enzyme that catalyses xanthine to urate

A

xanthine oxidase

286
Q

enzyme that catalyses hypo-xanthine to xanthine

A

xanthine oxidase

287
Q

enzyme that catalyses urate to allantoin

A

uricase

288
Q

does solubility of monosodium urate increase or decrease with temperature

A

decrease

289
Q

what happens to urate in the proximal convoluted tubule

A

reabsorbed then secreted

290
Q

what is Lesch-Nyhan syndrome

A

complete HGPRT deficiency

291
Q

symptoms of lesch-nyhan syndrome

A 
retardation
choreiform movements
self mutilation
spasticity
hyperuricaemia
developmental delay
292
Q

when do lesch-hyhan symptoms appear

A

developmental delay at six months
self mutilation at 1-16
choreiform movements at 1 yr

293
Q

causes of hyperuricaemia

primary causes of increased urate production

A 
Lesch nyhan syndrome
fructose intolerance
PRPP synthetase overactivity
partial HRPT deficiency
glycogen storage disorder
294
Q

causes of hyperuricaemia

secondary increased urate production

A 
myeloproliferative disorders
lymphoproliferative disorders
carcinomatosis
chronic haemolytic anaemia
Gaucher's disease
295
Q

causes of hyperuricaemia

primary causes of reduced urate excretion

A

FJHN

296
Q

causes of hyperuricaemia

secondary causes of reduced urate excretion

A 
Bartter syndrome
chronic renal failure
aspirin
diuretics
Downs
Saturine gout
297
Q

causes of hypouricaemia

decreased urate production

A

xanthine oxidase defiicency
allopurinol
liver failure

298
Q

causes of hypouricaeia

increased urate excretion

A

fanconi syndrome
idiopathic hypouricaemia
URAT1 inactivation
drugs

299
Q

joint most commonly affected in gout

A

1st MTP

300
Q

how to manage acute gout

A

NSAIDS
colchacine
glucocorticoids

301
Q

how to chronically mange gout

A

allopurinol
diet modification
drink lots of water
probenecid

302
Q

how to increase renal excretion of uric acid in chronic gout patients

A

probenecid

303
Q

what does allopurinal interact with

A

azothiprine

makes its intermediay 6-mercaptopurine last longer

304
Q

how to diagnose gout

A

Tap effusion
view under red polarised light
negatively bifringent crystals

305
Q

what is pseudogout

A

calcium pyrophosphate

306
Q

how to diagnose psuedogout

A

positively brifringent crystals under blue polarised light

307
Q

PCSK9 gain of function mutation inheritance

A

autosomal dominant

more LDL receptor degradation resulting in familial hypercholesterolaemia

308
Q

how to treat obesity

A

hypocaloric diet and exercise
orlistat
bariatric surgery

309
Q

metabolic acidosis abnormalities

A

low PH
high bicarbonate
low co2 if compensated

310
Q

causes of metabolic acidosis

A

increased H+ with reduced bicarbonate
increase H+ production: DKA
reduced H+ excretion: renal tubular acidosis
bicarbonate loss: intestinal fistula

311
Q

respiratory acidosis findings on ABG

A

raised CO2
raised H+
raised HCO3-

312
Q

causes of respiratory acidosis

A

poor ventilation
poor lung perfusion
impaired gas exchange

313
Q

metabolic alkalosis findings on ABG

A

reduced H+
increased bicarbonate
if compensted high pCO2

314
Q

causes of metabolic alkalosis

A

H+ loss: pyloric stenosis
hypokalaemia
bicarbonate ingestion

315
Q

findings on ABG for respiratory alkalosis

A

low H+
low CO2
low HCO3

316
Q

causes of respiratory alkalosis

A

artificial ventilation
voluntary
stimulation of respiratory centre

317
Q

what acidosis/ alkalosis does aspirin overdose cause

A

resp alkalosis

318
Q

criteria of a screening test

A 
Important health problem
Accepted treatment 
Facilities for diagnosis and treatment
Latent or early symptomatic stage
Suitable test or examination
Test should be acceptable to the population
Natural history understood
Agreed policy on whom to treat as patients
Economically balanced 
Continuing process
319
Q

in phenylketonuria where are abnormal metabolites found and what are they

A

phenylalanine in blood

phenylacetic acid in urine

320
Q

when is gunthrie test performed

A

day 5-8 of life

321
Q

urea cycle defects

A

HHH

Type 2 citrullinaemia

322
Q

what are urea cycle defects associated with

A

encephalopathy
respiratory alkalosis
irreversible neurological damage

323
Q

neonatal complications (common)

A 
retinopathy of prematureity
respiratory distress syndrome
PDA
Intraventricular haemmorhage
necrotising enterocolitis
324
Q

what is the pathology of necrotising enterocolitis

A

inflammation of the bowel wall leading to necrosis and perforation

325
Q

symptoms of necrotising enterocolitis

A

abdo distension

bloody stool

326
Q

signs of necrotising enterocolitis on AXR

A

intramural air

327
Q

when is full GFR reached

A

age 2

328
Q

what are the consequences of neonates not having complete GFR

A

limited ability to exchange Na+ for H+

slow excretion of solute load

329
Q

what is the difference in the proximal tubule between children and adults

A

shorter in children

330
Q

what is the significance of a shorter proximal tubule in children

A

LOWER RESORPTIVE CAPACITY but usually sufficient for small solute load

331
Q

what is the difference in the loop of henle and DCT between adults and children

A

shorter in children

332
Q

what is the difference in the loop of henle and DCT between adults and children

A

lower concentrating ability

333
Q

what is the maximum urine osmolarity in a child

A

700mmol/kg

334
Q

what is the difference in DCT between adults and children

A

DCT is comparitively unresponsive to aldosterone

335
Q

what changes occur in the volume of ECF in the first weeks of life

A

it falls by 40%

336
Q

cause of hypernatraemia in neonates

A

dehydration

salt poisoning

337
Q

how to differentiation causes of hypernatraemia in a neonate

A

paired urine/ blood creatine, urea and electrolytes

338
Q

what is the defect in congenital adrenal hyperplasia

A

21 hydroxylase deficiency

339
Q

what are symptoms of congenital adrenal hyperplasia

A

hyponatraemia
hyperkalaemia with volume depletion

hypoglycaemia
ambiguous genitalia in females
growth acceleration in children

340
Q

what hormones are lacking in congenital adrenal hyperplasia

A

aldosterone

cortisol

341
Q

causes of hyperbilirubinaemia (unconjugated bilirubine)

A 
increased synthesis (RBC breakdown)
increased enterohepatic circulation
low rate of transport into the liver
342
Q

what is the complication of hyperbilirubinaemia

A

bilirubin crosses BBB and causes kernicterus

343
Q

conditions causing hyperbilirubinaemia

A

crigler-najar syndrome
G6PD deficiency
haemolytic disease e.g rhesus/ abo incompatibility

344
Q

what is the definition of prolonged jaundice

A

14 days in term babies and 21 days in preterm babies

345
Q

causes of prolonged jaundice

A

breast milk jaundice
congenital hypothyroidism
neonatal infection/ sepsis

346
Q

what level of conjugated bilirubin is always pathological

A

> 20umol/L

347
Q

causes of conjugated hyperbilirubinaemia

A

biliary atresia
choledocal cyst
ascending cholangitis if TPN
galactosaemia (inherited metabolic disorders)

348
Q

what is conjugated hyperbilirubinaemia often associated with

A

cardiac abnormalities- situs inversus, polysplenia

349
Q

hypocalcaemia in a newborn can lead to

A

osteopenia of premaurity

fraying, splaying and cupping of long bones

350
Q

biochemistry of osteopenia

A

calcium is normal
phosphate is <1umol/L
alk phos> 1200U/L (10x adult ULN)

351
Q

how do you treat neonatal osteopenia

A

calcium and phosphate supplements

352
Q

presentation of rickets

A

bowing of legs, muscle hypotonia frontal bossing

353
Q

genetic causes of rickets

A

pseudovitamin D deficiency 1- defective receptors
pseudovitamin D deficiency 1- defective renal hydroxylation
familial hypophosphataemia

354
Q

familial phosphataemia

A

high urine phosphoethanolamine

low tubular maximal reabsorption of phosphate

355
Q

hyponatraemia after prostate surgery

A

TURP syndrome

flashcards of path guide 2018 (15 decks)

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