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Semester 5 April > Chemical Pathology > Flashcards

Chemical Pathology Flashcards

0
Q

How does estrogen appear in serum

A

Estradiol (ovaries) and estrone (from androstenedione in adipose)
60% albumin bound
38% SHBG
2% free (biologically active)

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1
Q

What favors Wolffian duct formation

A

Anti-Mullerian hormone

Testosterone

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2
Q

Define menopause

A

Permanent cessation of menstruation from loss of ovarian follicular fx for more than 12 months

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3
Q

Post menopausal woman are at more risk for…

A

CHD, osteoporosis

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4
Q

Causes of amenorrhea

A 
Outflow tract/uterus disorders (duct problems, androgen insensitivity, Asherman's)
Ovarian disorders (Turner's, premature ovarian failure) 
Pituitary disorders (prolactin secreting tumour, granulomatous infiltration, Sheehan's)
CNS disorders (Kallman's, craniopharyngioma, weight loss, stress, exercise)
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5
Q

Define hirsutism

A

Male pattern hair growth with hyperandrogenism often associated with menstrual irregularity

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6
Q

Why testosterone high in PCOS

A

Elevated androgens and insulin suppress hepatic SHBG synthesis = more free testosterone

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7
Q

Features of PCOS

A 
Menstrual irregularities 
Hyperandrogenism (hirsutism, acne, balding)
Obesity (50%)
Insulin resistance
Multiple follicles
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8
Q

Hormones in adrenal medulla are complexed to …

A

Proteins (chromogranins)

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9
Q

What analyte is measured in neuroblastoma (product of dopamine degradation)

A

Homovanillic acid

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10
Q

What regulates (nor)adrenalin release

A

Chronic - cortisol

Acute - acetylcholine causing Ca influx

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11
Q

Where is adrenalin synthesized

A

Chromaffin cell (adrenal medulla)

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12
Q

Most common cause of congenital adrenal hyperplasia

A

21-hydroxylase deficiency

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13
Q

Three forms of congenital adrenal hyperplasia

A

Simple virilising form
Severe salt losing form
Non-classical form (very mild -> ?infertility)

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14
Q

Define Addison’s disease

A

Primary adrenal hypofunction

Impaired ability to secrete cortisol and aldosterone

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15
Q

Key features of Addison’s

A

Orthostatic hypotension
Low Na
High K

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16
Q

Test for Addison’s

A 
Na, K, blood gas, renal functions
Baseline cortisol
ACTH levels (high in 1ry)

ACTH stimulation test (Synacthen test)
If Addison’s then poor cortisol response

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17
Q

What hormone can cause hyper pigmentation

A

ACTH

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18
Q

What drug can be used to treat pituitary tumour

A

Bromocrptine

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19
Q

Define gout

A

Recurrent inflammatory arthritis caused by deposition of monosodium urate crystals in synovial fluid

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20
Q

Pathogenesis of gout

A

Hyperuricaemia -> crystal deposition -> macrophage phagocytosis -> inflammatory cascade.

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21
Q

Causes of hyperuricaemia

A

Overproduction - enzyme defect, drugs(ethanol), obesity, malignancy, haemolytic disorders, myeloproliferative disorders.
Underexcretion - 1ry gout, diuretics, hypothyroid, hyperparathyroid, keto/lactic acidosis, renal insufficiency
Over consumption - meats, seafood, beer

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22
Q

Deficiency of hypoxanthine-guanine phosphoribosyltransferase

A

Lesch-Nyan syndrome

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23
Q

Prevention of gout

A

Decrease weight, alcohol, purine intake
Drugs - xanthine oxidase inhibitors (allopurinol), increase excretion (probenecid), increase uric acid metabolism (rasburicase)

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24
Q

Four characteristics of tumour lysis syndrome

A

Hyper - kalaemia, uricaemia, phosphataemia

Hypo - calaemia

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25
Q

Complications of hyperkalaemia

A

ECG changes
Cardiac arrhythmias
Vfib

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26
Q

Complications of hyperuricaemia

A

Acute renal failure
Kidney stones
Acute gout

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27
Q

Calcium decrease in tumour lysis due to

A

Binds proteins released by cells
Precipitates with phosphate
Long term: phosphate inhibits vitD activation

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28
Q

Complications of hypercalceamia

A

Cramps (tetany)
Convulsions
Cardiac arrhythmias

29
Q

Prevention of tumour lysis

A

IV hydration
Urine alkalinisation
Hypouricaemic agents (eg allopurinol, rasburicase)

30
Q

Treatment of tumour lysis syndrome

A

Kayexalate (decrease potassium)
Calcium replacement
Phosphate binders
DIALYSIS

31
Q

Define multiple myeloma

A

Malignancy of a single clone of plasma cells

32
Q

Causes of increased paraproteins

A

Myeloma/malignancy
Connective tissue disease
Primary amyloidosis
Benign conditions

33
Q

Light Ig chains found in urine

A

Bence-Jones proteins

34
Q

Clinical features of multiple myeloma

A

Bone infiltration = hypercalceamia, anaemia, osteolytic bone lesions, infection, bleeding.
Monoclonal proteins = elevated ESR, peripheral neuropathy, kidney failure, hyperviscosity syndrome

35
Q

Investigations for multiple myeloma

A

Protein electrophoresis
Immunotyping
Bence-Jones proteins
Free light chain ratio

36
Q

Causes of renal failure in multiple myeloma

A

Hypercalceamia - renal calcification
Hyperuricaemia
Light chain proximal tubal damage

37
Q

Counter regulatory hormones in glucose control

A

Glucagon
Adrenalin
Cortisol
Growth hormone

38
Q

Insulin causes

A

Glucose into cell (GLUT4)
Glycogen synthesis (inc glycogen synthase)
Protein synthesis
Fat synthesis/storage (inc Acetyl CoA carboxylate / lipoprotein lipase

Counters effects of counterreg hormones

39
Q

Mechanism of insulin release

A

Glucose binds GLUT 2 on pancreatic Bcells. Causes increase in ATP which causes reduced efflux of K leading to depolarization and influx of Ca. Ca influx causes insulin release.

40
Q

Define type 1 diabetes

A

B-cell destruction leading to absolute insulin deficiency

41
Q

Subcutaneous nodule found in hyperuricaemia

A

Tophus

42
Q

Define HbA1c

A

Non-enzymatic covalent glycation of the N-terminal valine on the beta chain of hemoglobin. Indications glucose level over RBC lifetime (120 days)

43
Q

Shortfalls of HbA1c

A

Increased RBC lifespan - iron deficiency, pregnancy, splenectomy, aplastic crisis
Decreased RBC lifespan - haemolytic disease, sickle cell trait, pregnancy, chronic blood loss.
Haemoglobinopathies

44
Q

Pathogenesis of DKA

A

No insulin.
Increase gluconeogenesis and glycogenolysis = hyperglycemia -> osmotic diuresis = dehydration.
Increased lipolysis = increased ketones = acidosis -> vomiting = dehydration

45
Q

Diagnosis of DKA

A

Low pH
High glucose
High ketone

46
Q

Pathogenesis of HONK

A

Low insulin.
Increased gluconeogenesis and glycogenolysis = hyperglycemia -> osmotic diuresis = dehydration. Increased blood viscosity = thrombosis. Increased plasma osmolarity = cerebral dehydration

47
Q

Diagnosis of HONK

A

Very high glucose >33
High osmolarity >320
N/decreased pH
NO KETONES

48
Q

What happens to K levels in DKA

A

K leaves cells in ketoacidosis (protein, glycolytic intermediates depleted and accumulating H displace K)
Excess intercellular K excreted by kidney.
Therefore, normal serum K despite profound decrease in intracellular K

49
Q

Treatment of DKA

A

Rehydrate (avoid cerebral oedema)
Monitor/replace intracellular ions
Administer insulin until normal pH

Treat predisposing cause eg infection

50
Q

Management of diabetes

A 
Diet
Exercise 
Manage complications
Oral hypoglycemic drugs
Insulin
51
Q

Causes of hypoglycemia

A 
LENDS
Liver disease
Endocrine disease (Addison's, GH def)
Neoplasms (insulinoma)
Drugs (insulin, alcohol)
Sepsis
52
Q

Define hypoglycemia

A

Glucose < 2.2 (<4.0 in diabetes)
Anxiety, weakness, faintness, headaches
Palpitations, tachycardia, sweating

53
Q

What tubes needed when measuring glucose + why

A

Sodium fluoride = inhibits metabolism

54
Q 
Where are each of these found
GLUT 1 
GLUT 2
GLUT 3
GLUT 4
A

RBC, brain
Liver, pancreatic Bcells
Neurons, placenta, brain
Muscle and adipose tissue

55
Q

Hormones that decrease appetite

A 
GLP 1
Oxymodulin
PYY
Insulin 
Leptin
56
Q

Hormone that increases appetite

A

Ghrelin

57
Q

Thyroid function tests

A 
TSH (screening test)
Free T4 (monitor Rx in known disease)
Free T3 (rarely tested - nonthyroidal illness, drugs, T3 toxicosis)
58
Q

Other thyroid tests

A

Thyroglobulin (thyroid cancer)
Calcitonin (medullary thyroid canc)
Thyroid Abs

59
Q

Causes of hyperthyroidism

A

Grave’s disease
Multinodular goitre
Toxic adenoma
Pituitary tumour

60
Q

Causes of hypothyroidism

A

Autoimmune (Hashimoto’s and atrophic thyroiditis)
Iatrogenic
Iodine deficiency
2ndry hypothyroidism

61
Q

Criteria needed to diagnose diabetes

A

Random blood glucose >11
Fasting glucose >7
OGT >11after 2 hours

62
Q

HbA1c normal range

A

4-6%

63
Q

Causes of microalbuminuria

A

Early diabetic nephropathy

Hypertension

64
Q

In cervical cancer what can cause anaemia?

A

Blood loss
Lack of erythropoietin from post renal failure
Anaemia of chronic disorders

65
Q

What compound does dipstix measure wrt ketones

A

Acetoacetate

66
Q

Options for lowering potassium and mechanisms

A

Kayexalate - cation binding resin
Loop diuretics + fluid = renal K loss
Glucose + insulin = glycolysis etc

67
Q

Reasons for urea increase but not creatinine

A

Pre renal failure

Accelerated protein catabolism

68
Q

Why LDH increased in leukaemia

A

Tumour derives energy from anaerobic glycolysis. Therefore glycolytic enzymes found in plasma

69
Q

Non malignant causes of isolated LDH increase

A

Haemolysis

Metaloblastic anaemia

70
Q

Metabolic derangements in alcohol abuse

A 
Hypertriglyceridemia
Ketosis
Hyperuricaemia 
Lactic acidosis
Hypoglycemia

Semester 5 April (17 decks)

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