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End Of Year > Chem Path > Flashcards

Chem Path Flashcards

0
Q

Interpretation of grey zone of PSA

A
  • 4-10
  • prostate carcinoma possible
  • benign conditions also cause elevations
  • should consider prostate biopsy
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1
Q

The physiological role of PSA

A

Liquifies seminal coagulum after intercourse, allowing sperm mobility

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2
Q

Benign causes for elevated PSA

A
  • prostatitis
  • BPH
  • urinary retention
  • catheterization
  • cycling
  • prostatic biopsy
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3
Q

Iron- related acute phase reactants - direction of change during inflam

A

Transferrin - decreased

Ferritin - increased

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4
Q

Test used in presence of inflam to identify iron deficiency anaemia

A

Soluble transferrin receptors

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5
Q

Relevance of excessive tea drinking

A
  • tea rich in tannins binds elemental iron in bowel lumen (preventing absorption)
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6
Q

Biochem and haematological markers of iron deficiency

A
  • low plasma iron
  • increased plasma transferrin
  • very low % saturation
  • low plasma ferritin
  • decreased Hb
  • microcytosis (decreased MCV)
  • low MCHC
  • hypo chromic microcytic cells on microscopy
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7
Q

Tests to distinguish acute iron poisoning from chronic overload

A
  • ferritin normal in acute, high in chronic overload

- transferrin normal in acute, low in chronic overload

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8
Q

Reason for increase in serum PSA 3 months after surgical prostate removal

A

Tumour recurrence/ metastasis

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9
Q

Significance of raised ALP with normal GGT in prostate cancer

A

Bone metastasis - increased osteoblast activity

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10
Q

Diagnostic value of serum free PSA estimation

A
  • when total PSA is in grey zone! the higher the serum free PSA, the less likely Ca prostate
  • because PSA secreted directly into blood is 100% bound to anti-chymotrypsin, but when PSA gains access via seminal vesicle (as per normal) a significant fraction is modified to no longer bind to anti-chymotrypsin and circulates in a free state
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11
Q

Why castration is option for inoperable prostate cancer

A
  • prostate cancer is often testosterone dependent

- removes major source of endogenous testosterone

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12
Q

An absolute contraindication for testosterone replacement in elderly hypo gonadal males

A
  • history of prostate cancer or raised PSA

- prostate cancer growth stimulated by testosterone

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13
Q

Lab tests to distinguish thalassemia from iron deficiency anaemia

A
  • serum iron
  • transferrin
  • ferritin
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14
Q

Why paracetamol selectively damages the liver

A

Metabolized via cytP450 to a reactive intermediate (NAPQI)

- targets free sulphydryl groups on intracellular proteins

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15
Q

Function of transferrin

A

Transports iron in circulation

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16
Q

Conditions with low transferrin

A
  • protein loss

- liver disease

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17
Q

Why not treat anaemia empirically

A

Prevent iron over load in non-iron deficient disorders (thalassemia)

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18
Q

Causes of raised INR

A
  • liver disease
  • vit k deficiency
  • warfarin
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19
Q

Why urea may be a misleading marker of renal function

A

Liver produces urea from ammonia

In liver failure, urea level may be lower than expected

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20
Q

Disorders in which excessive urobilinogen in urine

A
  • intra vascular haemolysis : lactate dehydrogenase

- hepatitis : transaminases

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21
Q

findings in a space-occupying mass within the liver

A
  • elevated ALP and GGT

- absence of jaundice

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22
Q

When would you find an elevated GGT on its own

A

Alcohol abuse, chronic drug ingestion

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23
Q

Useful biochemical tests for liver failure

A
  • plasma ammonia
  • abnormal INR
  • hypoglycemia
  • lactic acidosis
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24
Q

Clinical significance of bilirubin in urine

A

Obstruction to bile flow

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25
Q

Clinical significance of urobilinogen in urine

A

Haemolysis or intrinsic liver disease

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26
Q

Origin of ammonia in the body

A

Protein breakdown

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27
Q

What causes acute phase response

A

Any acute stress involving tissue necrosis

- cytokines relay to brain and live

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28
Q

Positive acute phase reactants

A
  • CRP
  • a1 antitrypsin
  • fibrinogen
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29
Q

Negative acute phase reactants

A
  • albumin
  • transferrin
  • HDL
  • LDL
30
Q

Mechanism of lactic acidosis

A
  • hypoxia to any tissue disrupts mitochondrial metabolism
  • pyruvate metabolism not possible
  • LDH forms lactic acid
31
Q

Causes of pre-renal failure

A
  • hypovolaemia
  • decrease cardiac output
  • renovascular obstruction
32
Q

Causes of intra renal failure

A
  • acute tubular necrosis
  • acute glomerular nephritis
  • interstitial nephritis
  • intra renal vasoconstriction
  • tubular obstruction
33
Q

Causes of post renal failure

A
  • bilat ureteric obstruction

- urethral obstruction

34
Q

Why urgent to decide between pre and intra renal

A
  • pre can progress rapidly to more serious intra renal failure
  • some treatment options for intra are opposite to pre
35
Q

When to dialyse a patient

A
  • volume overloaded at risk of pulm oedema or cardiac failure
  • blood urea >50 and rising
  • K high/ECG changes
  • bicarb lower than 10
36
Q

Definition of a buffer

A

Solution of conjugate acid-base pair

37
Q

Causes of resp acidosis

A
  • depression of resp centre
  • physical inability to ventilate
  • airway obstruction
  • pulm disease causing decreased exchange
38
Q

Causes of resp alkalosis

A
  • direct stim of resp centre
  • mech over ventilation
  • hypoxia
39
Q

Causes of metabolic acidosis

A
  • gain of H

- loss of bicarb (anion gap normal)

40
Q

Causes of metabolic alkalosis

A
  • gain of bicarb

- loss of H

41
Q

Requirements before a fasted lipid profile can be done

A
  • stable diet for more than 2 weeks
  • alcohol abstinence for 48hrs
  • fast overnight
  • sit for 5 mins before venesection (min tourniquet time)
42
Q

Reasons for raised anion gap

A
  • alcohol
  • uraemia
  • diabetic ketoacidosis
  • drugs
  • lactate
43
Q

Requirements for reliable blood gas result

A
  • arterial blood
  • anticoag with heparin
  • taken and kept anaerobic
  • on ice
  • analysed ASAP
44
Q

AMI markers

A
  • myoglobin (stores O2)
  • creatine kinase (stores energy as creatine kinase)
    A
  • troponin (part of contractile apparatus)
45
Q

Acquired causes of hypercholsterolaemia

A
  • hypothyroidism
  • nephrotic syndrome
  • diabetes mellitus
46
Q

Role of DMT1

A

Transports iron from gut into cell in reduced form

47
Q

Role of ferroportin

A

Transports iron out of cell

- inhibited by hepcidin

48
Q

Role of hephaestin

A
  • copper-containing protein on basolateral membr of gut cells
  • oxidizes iron to Fe3 so it can be transported by transferrin
49
Q

Role of caeruloplasmin

A
  • copper-containing protein in circulation (macs)

- oxidizes iron to fe3 so it can be transported by transferrin

50
Q

Role of transferrin

A

Transporter of 2x Fe3 atoms in the blood

  • normally 30% sat
  • synthesised by liver
51
Q

Role of transferrin receptors

A
  • bind iron bound transferrin and internalises transferrin

- increases with iron demand

52
Q

Role of hepcidin

A

Inhibits ferroportin leading to

  • accumulation of iron in RES and liver
  • decreased iron uptake by GIT
53
Q

Treatment if acute iron toxicity

A
  • resuscitation

- chelation with desferrioxanine

54
Q

Description of hereditary haemochromatosis

A
  • mutation in HFE protein leads to decrease in hepcidin synthesis
  • iron stores accumulate in parenchyma
55
Q

Cells affected first by folate deficiency

A
  • blood cell precursors in BM
  • mucosal cells of intestine
  • rapidly growing fetus
56
Q

People at risk for folate deficiency

A
  • intestinal disease (malabsorption)
  • pregnant women
  • patients on anti-folate chemotherapeuric drugs
57
Q

SAM needed for

A
  • synthesis of neurotransmitters like ACh

- synthesis of phospholipids used to make myelin

58
Q

Biochem reactions for which vit b12 is an essential cofactor

A
  • methionine synthase

- methylmalonyl mutate (krebs cycle)

59
Q

How to diagnose b12 deficiency

A
  • elevated total homocysteine

- elevated urinary methylmalonic acid

60
Q

Causes of intra vascular haemolysis

A
  • autoimmune
  • mechanical (heart valves)
  • infectious (malaria)
  • inherited red cell fragility
  • osmotic
61
Q

Signs of intravascular haemolysis

A
  • increase unconjugated BR
  • increased conj BR and urobilinogen in urine
  • increased LDH and AST in plasma
  • decreased haptoglobin
  • schistocytes on peripheral blood smear
  • haemoglobinuria
62
Q

How to know it’s not intravascular but extra vascular haemolysis

A
  • no increased unconjugated BR

- often raised potassium

63
Q

How to prevent extravascular haemolysis

A
  • avoid tiny needles
  • avoid high vacuum
  • avoid drawing blood rapidly through long thin lines
64
Q

2 types of porphyria

A
  • porphyrinogens spontaneously oxidized to porphyrins (reactive to UV, oxygen radicals damage skin)
  • massive build up of PBG and dALA (mimic neurotransmitters - acute attacks)
65
Q

Things that can trigger acute porphyria attacks

A
  • onset of puberty
  • fasting carb depletion
  • drugs and alcohol
66
Q

Characteristics of an acute attack

A
  • abdo pain
  • sensory and motor neuropathy
  • autonomic neuropathy
  • CNS (anxiety)
  • hyponatraemia (vomiting)
67
Q

Management of acute attack

A
  • make diagnosis (PBG and ALA in urine)
  • don’t operate
  • push glucose
  • ascertain fluid balance and slowly correct hyponatraemia
  • get expert advice
  • get into ICU and ventilate
68
Q

Screening test for acute attack of porphyria

A
  • 1ml freshly voided urine
  • add 1ml Erlich’s aldehyde
  • mix
  • pink/red color implies presence of urobilinogen
  • add 2ml chloroform
  • mix and allow to settle
  • PBG remains in top layer
69
Q

PSA measurement good for

A
  • progression of tumour
  • response to therapy
  • screening
70
Q

Things to measure to improve PSA specificity

A
  • PSA density
  • PSA velocity
  • % free
  • complexed PSA
71
Q

Characteristics of a good tumour marker

A
  • normally absent
  • no false positives (specific) and no false negatives (sensitive)
  • long time before clinical presentation
  • specific for particular tumour
  • correlates with tumour mass and stage
  • prognostic value
  • easily measured
  • treatment exists
72
Q

Important considerations when assessing pituitary function

A
  • negative feedback
  • cyclical fluctuations
  • effect of stress
  • effect of intense exercise
  • effect of development
73
Q

Major actions of growth hormone

A
  • antagonists insulin (promotes lipolysis)

- stimulates production of insulin like GH1 (inhibits protein breakdown)

End Of Year (12 decks)

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