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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
Four characteristics of tumour lysis syndrome
Hyper - kalaemia, uricaemia, phosphataemia | Hypo - calaemia
25
Complications of hyperkalaemia
ECG changes Cardiac arrhythmias Vfib
26
Complications of hyperuricaemia
Acute renal failure Kidney stones Acute gout
27
Calcium decrease in tumour lysis due to
Binds proteins released by cells Precipitates with phosphate Long term: phosphate inhibits vitD activation
28
Complications of hypercalceamia
Cramps (tetany) Convulsions Cardiac arrhythmias
29
Prevention of tumour lysis
IV hydration Urine alkalinisation Hypouricaemic agents (eg allopurinol, rasburicase)
30
Treatment of tumour lysis syndrome
Kayexalate (decrease potassium) Calcium replacement Phosphate binders DIALYSIS
31
Define multiple myeloma
Malignancy of a single clone of plasma cells
32
Causes of increased paraproteins
Myeloma/malignancy Connective tissue disease Primary amyloidosis Benign conditions
33
Light Ig chains found in urine
Bence-Jones proteins
34
Clinical features of multiple myeloma
Bone infiltration = hypercalceamia, anaemia, osteolytic bone lesions, infection, bleeding. Monoclonal proteins = elevated ESR, peripheral neuropathy, kidney failure, hyperviscosity syndrome
35
Investigations for multiple myeloma
Protein electrophoresis Immunotyping Bence-Jones proteins Free light chain ratio
36
Causes of renal failure in multiple myeloma
Hypercalceamia - renal calcification Hyperuricaemia Light chain proximal tubal damage
37
Counter regulatory hormones in glucose control
Glucagon Adrenalin Cortisol Growth hormone
38
Insulin causes
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
Mechanism of insulin release
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
Define type 1 diabetes
B-cell destruction leading to absolute insulin deficiency
41
Subcutaneous nodule found in hyperuricaemia
Tophus
42
Define HbA1c
Non-enzymatic covalent glycation of the N-terminal valine on the beta chain of hemoglobin. Indications glucose level over RBC lifetime (120 days)
43
Shortfalls of HbA1c
Increased RBC lifespan - iron deficiency, pregnancy, splenectomy, aplastic crisis Decreased RBC lifespan - haemolytic disease, sickle cell trait, pregnancy, chronic blood loss. Haemoglobinopathies
44
Pathogenesis of DKA
No insulin. Increase gluconeogenesis and glycogenolysis = hyperglycemia -> osmotic diuresis = dehydration. Increased lipolysis = increased ketones = acidosis -> vomiting = dehydration
45
Diagnosis of DKA
Low pH High glucose High ketone
46
Pathogenesis of HONK
Low insulin. Increased gluconeogenesis and glycogenolysis = hyperglycemia -> osmotic diuresis = dehydration. Increased blood viscosity = thrombosis. Increased plasma osmolarity = cerebral dehydration
47
Diagnosis of HONK
Very high glucose >33 High osmolarity >320 N/decreased pH NO KETONES
48
What happens to K levels in DKA
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
Treatment of DKA
Rehydrate (avoid cerebral oedema) Monitor/replace intracellular ions Administer insulin until normal pH Treat predisposing cause eg infection
50
Management of diabetes
``` Diet Exercise Manage complications Oral hypoglycemic drugs Insulin ```
51
Causes of hypoglycemia
``` LENDS Liver disease Endocrine disease (Addison's, GH def) Neoplasms (insulinoma) Drugs (insulin, alcohol) Sepsis ```
52
Define hypoglycemia
Glucose < 2.2 (<4.0 in diabetes) Anxiety, weakness, faintness, headaches Palpitations, tachycardia, sweating
53
What tubes needed when measuring glucose + why
Sodium fluoride = inhibits metabolism
54
``` Where are each of these found GLUT 1 GLUT 2 GLUT 3 GLUT 4 ```
RBC, brain Liver, pancreatic Bcells Neurons, placenta, brain Muscle and adipose tissue
55
Hormones that decrease appetite
``` GLP 1 Oxymodulin PYY Insulin Leptin ```
56
Hormone that increases appetite
Ghrelin
57
Thyroid function tests
``` TSH (screening test) Free T4 (monitor Rx in known disease) Free T3 (rarely tested - nonthyroidal illness, drugs, T3 toxicosis) ```
58
Other thyroid tests
Thyroglobulin (thyroid cancer) Calcitonin (medullary thyroid canc) Thyroid Abs
59
Causes of hyperthyroidism
Grave's disease Multinodular goitre Toxic adenoma Pituitary tumour
60
Causes of hypothyroidism
Autoimmune (Hashimoto's and atrophic thyroiditis) Iatrogenic Iodine deficiency 2ndry hypothyroidism
61
Criteria needed to diagnose diabetes
Random blood glucose >11 Fasting glucose >7 OGT >11after 2 hours
62
HbA1c normal range
4-6%
63
Causes of microalbuminuria
Early diabetic nephropathy | Hypertension
64
In cervical cancer what can cause anaemia?
Blood loss Lack of erythropoietin from post renal failure Anaemia of chronic disorders
65
What compound does dipstix measure wrt ketones
Acetoacetate
66
Options for lowering potassium and mechanisms
Kayexalate - cation binding resin Loop diuretics + fluid = renal K loss Glucose + insulin = glycolysis etc
67
Reasons for urea increase but not creatinine
Pre renal failure | Accelerated protein catabolism
68
Why LDH increased in leukaemia
Tumour derives energy from anaerobic glycolysis. Therefore glycolytic enzymes found in plasma
69
Non malignant causes of isolated LDH increase
Haemolysis | Metaloblastic anaemia
70
Metabolic derangements in alcohol abuse
``` Hypertriglyceridemia Ketosis Hyperuricaemia Lactic acidosis Hypoglycemia ```

Semester 5 April (17 decks)

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