Pathology Block I Diseases

Front 1

Fatty Change (Steatosis)

Back 1

Accumulation of TGs, usu. in hepatocytes. Potentially reversible. Causes: toxins (ethanol), protein malnutrition, diabetes mellitus, obesity, overeating, hypoxia.

Front 2

Atherosclerosis

Back 2

Accumulation of cholesterol/CEs within sm mm and macs. (extracellular accumulations can also occur)

Front 3

Spongiform Encephalopathy

Back 3

A prion disease of α-helical to abnormal β-pleated sheets.

Front 4

Haemosiderosis

Back 4

Mild accumulation of iron (pigment) haemosiderin with no damage or impairment.

Front 5

Haemochromatosis

Back 5

Marked accumulation of iron pigment with damage to:
Organs: liver, pancreas, heart, skin, endocrine.
Sxs: liver dysfunction (cirrhosis), DM, ↑skin pigmentation.

Front 6

1° Haemochromatosis

Back 6

Genetic due to mutation in short arm of chr. 6 causing ↑ intestinal absorption.

Sxs: Cirrhosis, DM, skin pigmentation. "Bronze diabetes".

Front 7

2° Haemochromatosis

Back 7

Non-hereditary; most common cause is haemolytic anaemia associated with blood transfusions and ineffective ↑erythropoiesis. Presents in middle-age.

Assoc. sx: Pitting oedema, spider angioma, gynectomastia, diabetes,

Front 8

Dystrophic Calcification

Back 8

Pathologic depositon of calcium in necrotic/damaged tissue with normal serum [Ca2+].

Calcification is basophilic

Front 9

Metastatic Calcification

Back 9

Pathologic deposition of Ca2+ in normal tissue, assoc. with hypercalcaemia, hyperparathyroidism, excessive vit. D.

Calcification is basophilic

Front 10

2° Hyperparathyroidism

Back 10

Usually associated with chronic renal failure.

Front 11

Multiple Myeloma (plasma cell neoplasm)

Back 11

Amyloidotic disease

Precursor: Ig light chains
Major fibril: AL

Systemic manifestations

Front 12

Inflammatory Amyloidosis (eg. Rheumatoid Arthritis)

Back 12

Amyloidotic diseases

Precursor: SAA (serum amyloid associated protein, syn.'d by liver)
Major fibril: AA

Systemic Manifestations

Front 13

Alzheimer's Disease

Back 13

Amyloidotic disease

Precursor: APP (amyloid precursor protein)
Major fibril: Aβ

Localised cerebral plaques

Front 14

Benign Prostatic Hyperplasia

Back 14

Acinar epithelial, sm mm, and stromla fibroblasts all can experience hyperplasia due to hormonal stimulation. Key histologic feature is papillary infoldings of glandular epithelium.

Front 15

Ischemic/Hypoxic Cell Damage

Back 15

Chain of Events:
1.) ↓ Na-K pump
2.) Hydropic Change due to net Na+ gain.
3.) Shift to glycolysis, lactic acid buildup (pH ↓)
4.) Ca2+ enters cell, activates phospholipases, ATPases, proteases, endonucleases.
5.) mt damage by free radicals, protein syn. stops.

Front 16

Progeria (Hutchinson-Gilford Syndrome)

Back 16

Defect: De novo mutation in the lamin A gene activates a cryptic splice site; abnormal nuclear mem,

Sxs: premature aging, death by age 13. IQ is normal though.

Onset: Early childhood,

Tx: Farnesyltransferase inhibitors

Front 17

Werner's Syndrome

Back 17

Defect: Mutation in WRN gene, a DNA helicase.

Onset: 2nd/3rd decade of life.

Sx.: Succumb to age-assoc. pathologies (cancer, diabetes, cataracts, etc) 5 years after onset.

Front 18

Acute Inflammation

Back 18

Minutes to few days.
Causes: Infxn, infarction, trauma.
Events: Vasodilation (arteriolar side), ↑perm (venule side), vascular stasis, leukocyte extravasation, phagocytosis.
First 24hrs: neutrophils
24-48hrs: macs

Front 19

Chronic Inflammation

Back 19

Weeks to years
Causes: persistant infxns, prolonged exposure to irritants/toxins, autoimmunity.
Events: Macs cause enzymatic destruction, attract other cells, fibroblast proliferation, and angiogenesis. Mast cells contribute.

Front 20

Granulomatous Inflammation

Back 20

Special form of chronic inflammation.
Causes: TB, Histoplasma capsulatum, sutures, lipids.
Features: Caseation often seen in centre, surrounded by epithelioid macs, surrounded by lymphocytes.

Front 21

Pitting Oedema

Back 21

Caused by ↓'d plasma oncotic pressure from ↓'d albumin syn.; indicative of liver dysfunction.

Front 22

Ehler-Danlos Syndrome,
Osteogenesis Imperfecta

Back 22

Diseases of collagen malformation

Front 23

Marfan Syndrome

Back 23

Defect: Fibrillin (component of elastic fibres)

Front 24

Pulmonary Oedema

Back 24

A potentially fatal form of odema which impairs resp.

Front 25

Brain Oedema

Back 25

Potentially fatal odema; swelling withing confined skull leads to herniation, impairment of blood flow, and disruption of brain stem.

Front 26

Congestive Heart Failure

Back 26

C.O. inadequate to meet met. demands of the body. Most commonly due to ischemic heart disease. Also due to HTN, inability to fill chambers.

Front 27

Left-sided Failure

Back 27

Results in pulmonary congestion/oedema and ↓'d renal perfusion. Leads to prerenal azotaemia (↓'d protein excretion), activation of reinin-ATN-aldo sys.

Front 28

Right-sided Failure

Back 28

Systemic/portal venous congestion, causing impairment of liver fxn.

Front 29

Haematoma

Back 29

accumulated blood within a tissue or space

Front 30

Petechiae

Back 30

Minute haemorrhages (1-2mm)

Front 31

Purpura

Back 31

Medium-sized haemorrhages (≤1cm)

Front 32

Ecchymoses

Back 32

Large, blotchy haemorrhage

Front 33

Haemothorax

Back 33

haemorrhage into pleural cavity

Front 34

Haemopericardium

Back 34

Haemorrhage into pericardial sac; will crowd the heart, preventing proper pumping (CHF)

Front 35

Haemoperitoneum

Back 35

Haemorrhage into peritoneal cavity

Front 36

Haemoarthrosis

Back 36

Haemorrhage into joint space.

Front 37

Contusion (bruise)

Back 37

Haemorrhage within tissue following rupture of small BV by blunt trauma.

Front 38

Hypovolaemic shock

Back 38

Shock due to excessive fluid loss/haemorrhage.

Front 39

Cardiogenic shock

Back 39

shock due to ↓'d C.O.

Front 40

Neurogenic shock

Back 40

shock due to deranged peripheral vasomotor control from NS injury. Mechanism similar to shock caused by sepsis, drugs, and anaphylaxis.

Front 41

Septic Shock

Back 41

Usu. due to gram neg bacilli endotoxin (LPS), causing 2° release of vasodilating and pro-coagulating cytokines

Front 42

Acute Tubular Necrosis

Back 42

Renal manifestation of decompensated shock.

Front 43

Centrolobular Necrosis

Back 43

Hepatic manifestation of decompensated shock, because that's where the blood is most deoxygenated.

Front 44

filariasis

Back 44

parasitic worm that enters and blocks lymph vessel, causing localised oedema.

Front 45

Classic Haemophilia (Haemophilia A)

Back 45

Factor VIII deficiency due to lack of vWf to transport it. Intrinsic pathway impaired.

Caused by inversion of a gene on X-chr. in about half of cases.

Front 46

Christmas Disease (Haemophilia B)

Back 46

Factor IX deficiency (intrinsic pathway)

Front 47

Thrombophilia

Back 47

Easy to clot; inherited cases due to mutant factor V-Leiden that's resistant to protein C, or dysfunction of protein C, S or antithrombin.

Front 48

Cri du chat syndrome

Back 48

(5p- syndrome)
Sxs: mental retardation, developmental abnormalities.

Front 49

13q- syndrome

Back 49

↑'d susceptibility to neoplasm retinoblastoma, etc. Two-hit hypothesis.

Front 50

Subtelomeric deletion/rearrangement

Back 50

seen in some cases of mental retardation with dysmorphic features. Assayed with FISH or CGH (comparative genomic hybridisation)

Front 51

Burkett's Lymphoma

Back 51

Transcriptionally active gene gets translocated next to oncogene. Same mechanism as Chronic Myelocytic Leukaemia.

Front 52

Turner Syndrome

Back 52

Monosomy X; can be caused by Robertsonian Translocation (monosomic for short arm.)
Sxs: short stature, 1° amenorrhea, shield chest, webbed neck, low hairline, thyroiditis, HTN.
↑risks: 15% coarctation of aorta.
High incidence of mosaicism, 10% of 1st trimester miscarriages.

Front 53

Down Syndrome

Back 53

Trisomy 21, usu. due to nondisjunction, or rarely a balanced Robertsonian Translocation. 1% are mosaics.
Dx: low α-foetoprotein, estriol, high β-hCG, inhibin A.
Sxs: hypotonia, flat facial profile, epicanthal folds, oblique palpebral fissures.
↑risks: 1/3 have serious cardiac malformations. 3% have intestinal obstruction. 15x risk of childhood leukaemia.

Front 54

Klinefelter's Syndrome

Back 54

47XXY
Sxs: weak facial hair, gynectomastia, female fat distr., infertility, long legs, hyalinised tubules.
↑risks: breast cancer.

Front 55

Cystic Fibrosis

Back 55

Deletion/mut. of CFTR gene, for regulationof epithelial Cl- transport. 70% pts. N. European, 4-bp del.
Dx: Sweat Cl- test screens for most common 20-23 muts.
Sxs: worsening pulmonary fxn, repeated infxns, rt. heart failure (cor pulmonae), death by hepatobiliary disease. Med. survival is 35 yrs.
↑risks: 10% meconium ileus, bronchiolitis, bronchitis, bronchiectasis, recurrent pneumonia, chronic pancreatitis, steatorrhea, azospermia.

Front 56

Gaucher Disease

Back 56

Class: Sphingolipidosis Single base mut. in β-glucosidase. Glucosylceramide accumulates in mac lysosomes.
Dx: foamy spleen cells
Sxs: splenomegaly, anaemia, leukopaenia, thrombocytopaenia.

Front 57

Type 1 Gaucher Disease

Back 57

Adult onset, most common. Normal lifespan. Bone involvement can lead to disability. Suppl. with I.V. acid glucose cerebrosidase possible but expensive.

Front 58

Type 2 Gaucher Disease

Back 58

Childhood onset, rapid deterioration, most die before year 1.
Sxs: hepatosplenomegaly and neurological abnormalities.

Front 59

Type 3 Gaucher Disease

Back 59

Similar to Type 2 with neurological deterioration, but slower progression.

Front 60

Phenylketonuria (PKU)

Back 60

Mut. for gene for Phe Hydroxylase (PAH)
Sxs: Fair skin, blonde hair, blue eyed (can't make melanin), "mousy odour" due to phenylacetic acid. Progresses to mental retardation.
Dx: AA analysis of urine/plasma.
Tx: Strict dietary restriction of Phe for pregnant mother, then child.

Front 61

Neurofibromatosis-1 aka von Recklinghausen Disease

Back 61

Defect: NF-1 tumour suppressor gene. Half cases are sporadic, others familial.
Sxs: cafe-au-lait skin lesions, multiple neurofibromas, Lisch nodules (iris hamartomas), ↑ risk of other neurogenic tumours.

Front 62

Polycystic Kidney Disease

Back 62

Defects: PKD1 gene (85%), or PKD2, rarely PKD3. Affects renal epithelial cilia.
Sxs: haematuria, HTN, abdominal pain/mass, renal failure (cause of death).
Onset: 3rd to 5th decade of life.
Dx: CT/ultrasound
Assoc.: hepatic cysts (33%), intracranial (berry) aneurysms.

Front 63

Duchenne Muscular Dystrophy

Back 63

Defect: dystrophin gene del, larger del = worse disease. X-linked.
Sxs: initial clumsiness, progressive muscular weakness, waddling gait, eventual wheelchair dependence. Death age 14-20 due to resp. insufficiency, cardiac decompensation.
Dx: ↑serum CK

Front 64

Fragile X Syndrome

Back 64

Defect: X-chr. CGG repeat in FMR-1 gene (fragile site)
Sxs: mental retardation, post-pubertal macro-orchidism, large ears, square chin, large mandible, long face.
Dx: southern blot or PCR to demonstrate repeat size.
Notes: exhibits anticipation

Front 65

Kearns-Sayre Syndrome

Back 65

Mitochondrial disorder

Front 66

MELAS

Back 66

Mitochondrial disorder; "Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes".

Front 67

MERRF

Back 67

"Myoclonic epilepsy with ragged-red fibres"; a mitochondrial disease.

Front 68

Leber Hereditary Optic Neuropathy

Back 68

Mitchondrial disorder

Front 69

Prader-Willi Syndrome

Back 69

Defect: del on paternal chr. 15q11-13, subsequent inactivating methylation of maternal copy.

Sxs: hypotonia, obesity, hypogonadism, mental retardation

Front 70

Angelman Syndrome

Back 70

Defect: del of maternal 15q11-13, subsequent inactivating methylation of paternal copy.
Sxs: hyperactivity, inapproriate laughter, severe mental retardation.

Front 71

Kwashiorkor

Back 71

Class: protein malnuturition
Sxs: apathy, peripheral oedema, enlarged fatty liver, anaemia.
Notes: seen in third-world countries where children are weened too early to make room for next sibling.

Front 72

Marasmus

Back 72

aka starvation, general deficiency of calories.
Sxs: stunted growth, loss of subcutaneous fat, atrophy of mm, prematurely aged appearancce.

Front 73

Cachexia

Back 73

Class: 2° protein-energy malnutrition; seen in cancer, AIDS, post-op. "Wasting away".

Front 74

Anorexia Nervosa

Back 74

self-imposed starvation (cf. marasmus), esp. in young women.
Sxs: amenorrhea, ↓TH, anaemia, lymphopaenia, hypoalbuminaemia, hypokalemia (↑risk cardiac arrythmia)

Front 75

Vitamin A deficiency

Back 75

2°: fat malabsorption.
Sxs: Night blindness, epithelial abnormalities (squamous metaplasias, keratomalacia [corneal softening], xerophthalmia[dry eyes]), ↑risk childhood infxns

Front 76

Scurvy

Back 76

Vitamin C deficiency
Sxs: (All related to collagen malsynthesis)haemorrhages, subperiosteal haematomas, sk changes, impaired wound healing.

Front 77

Vitamin E deficiency

Back 77

Cause: usu. caeliac disease, CF, or liver disease (fat malabsorption).
Sxs: neurologic damage (degeneration of post. column, neurone loss from DRG), pigmented retinopathy, sk mm disease.

Front 78

Wet Beriberi

Back 78

Thiamine (B1) deficiency
Alcoholics, gastric bypass pts.
Sxs: Cardiac sxs; may have oedema, myofibre swelling, and ind. myocyte necrosis.

Front 79

Dry Beriberi

Back 79

Thiamine (B1) deficiency
Sxs: Peripheral nn sxs; symmetric polyneuropathy in feet and lower legs. Spreads proximally over time. Demyelination, axonal disruption (in severe cases)

Front 80

Wernicke-Korsakoff Syndrome

Back 80

Thiamine (B1) deficiency seen mostly in alcoholics.
sxs: Haemorrhage/necrosis of mammillary bodies and specific areas of the brain. Leads to dementia, ataxia, global confusion, ophthalmoplegia, and nystagmus. Also marked memory loss.

Front 81

Iron Deficiency

Back 81

Causes: heavy menstrual flow, internal/GI haemorrhage, kids fed only milk after 6 months
Assoc.: hypochromic microcytic anaemia. Brain/developmental abnormalities in children.

Front 82

Zinc Deficiency

Back 82

Cause: usu. unsupplemented TPN, or congenital metal ion transporter deficiency.
Sxs: skin rash (acrodermatitis enteropathica), growth retardation, infertility

Front 83

Selenium Deficiency

Back 83

Cause: usu. unsupplemented TPN
Assoc.: congestive cardiomyopathy

Front 84

Iodine Deficiency

Back 84

Sxs: hypothyroidism, goiter. Iodine deficient mother can give birth to child with congenital hypothyroidism, progressing to cretinism (retardation)

Front 85

Metabolic Syndrome

Back 85

"Syndrome X", consisting of insulin resistence, dyslipidaemia, HTN, abdominal obesity, proinflammatory state (due to fatty liver?), prothrombotic state.

Front 86

Nonalcoholic steatohepatitis (NASH)

Back 86

fatty change in liver assoc. with Type II diabetes. May progress to cirrhosis.

Front 87

Obesity

Back 87

BMI ≥ 30
↑risk: metabolic syndrome, NASH, cholelithiasis (gallstones), osteoarthritis, lower back pain, ischaemic stroke, venous thrombosis.

Front 88

Copper Deficiency

Back 88

Cause: rare; usu. with TPN.
Sxs: anaemia, poor wound healing, mm weakness

Front 89

Benign Neoplasm

Back 89

1.) pushing, not invading borders.
2.) No metastasis
3.) Closely resembles tissue of origin

Front 90

Malignant Neoplasm

Back 90

1.) Infiltrating, invading borders
2.) Metastisis to distant sites
3.) Can resemble tissue of origin, or be poorly/undifferentiated (pleomorphism)

Front 91

Chronic Myelocytic Leukaemia (CML)

Back 91

Defect: Reciprocal t(9:22); transcriptionally active bcr gene fuses with abl oncogene to produce fusion Tyr kinase.
Onsent: middle age
Sxs: fatigue, wt. loss, night sweats, 40% asymmptomatic.
Dx: PCR using bcr-abl as primer.
Tx: Gleevec (Imatinib mesylate) Tyr Kinase inhibitor specific for bcr-abl

Front 92

CML - chronic phase

Back 92

Phase I of CML; ↑ leukocyte, platelet count, <10% myeloblasts; bone marrow hypercellular, dominated by myeloid cells.

Front 93

CML - accelerated phase

Back 93

Phase II of CML: ≤20% myeloblasts, ≤basophils, splenomegaly, rising white count unresponsive to therapy.

Front 94

CML - blast phase

Back 94

Phase III (final) of CML: ≥20% myeloblasts, extramedullary deposits of leukaemic blasts, resembles acute leukaemia, poor prognosis.

Front 95

Hereditary Nonpolyposis Colon Cancer (HNPCC)

Back 95

Defect: DNA mismatch repair gene, such as hMSH2 (a mutator gene), loss of fxn due to two-hit leads to genomic instability
Onset: as early as young adulthood.
Sxs: Accounts for 5% of all colon cancers.

Front 96

Familial Adenomatus Polyposis (FAP)

Back 96

Defect: mutated APC (tumour suppressor) gene fails to bind β-catenin to target for degradation. ↑'d β-catenin stimulates transcription of cell prolif. genes.
Sxs: hundreds to thousands of colon polyps.

Front 97

Xeroderma Pigmentosum

Back 97

Autosomal recessive with defect in nucleotide excision repair of pyrimidine dimers due to UV damage.

Front 98

Malignancy

Back 98

Sxs: anorexia, wt. loss, fever (TNF-α, IL-1, IFN-γ), distant effects (paraneoplastic syndromes)

Front 99

Cushing Syndrome

Back 99

Paraneoplastic syndrome of small cell carcinoma of lung, and carcinoid tumours.

Front 100

Acetaminophen Toxicity

Back 100

Tylenol detox'd by sulfation and glucuronidation in liver by reduced GSH. Overdose depletes GSH, toxic metabolites accumulate. Massive centrolobular hepatic necrosis 3-5d after.
Tx: acetyl cysteine, or pump stomach if within 12h.
Notes: Alcohol will tie up GSH, ↓g tolerance for tylenol.

Front 101

CO Poisoning

Back 101

CO: odourless, nonirritating gas from engine exhaust, fires, heating, cigarette smoke. CO affinity for Hb 200x > than O2.

Front 102

HCN (Cyanide) Poisoning

Back 102

HCN (Hydrogen Cyanide) is rapidly absorbed via bronchia mucosa and alveoli, effects within sec/mins. Blocks cyt oxidase, diffuse cellular anoxia. Almonds?

Front 103

Mercury Poisoning

Back 103

Hg binds covalently to sulfhydryl groups, denaturing proteins and inactivating enzymes.

Front 104

Inorganic (HgCl, etc) Mercury poisoning

Back 104

Not absorbed through the skin, only inhaled as vapour.
Effects: acute: proximal tubular necrosis.
Chronic: nephritic syndrome.

Front 105

Elemental/organic Mercury Poisoning

Back 105

Absorbed across skin and BBB, causes neuronal injury/necrosis.

Front 106

Lead Poisoning

Back 106

Pb inhibits δ-aminolevulinic acid (↓haeme syn.), Na-K ATPase (↑RBC fragility), mt ox-phos (neuronal loss).
Targets: Kidneys, marrow, PNS (adults), brain (children), GI,

Front 107

Silicosis

Back 107

Class: pneumoconiosis
Cause: inhalation of silica (quartz) from mining, stonecutting, polishing, sandblasting, foundry work, ceramics.
Onset: 15-20+ exposure
Path: macs secrete fibrogenic/chemotactic factors in response, creating collagneous nodule. Nodules may coalesce into large fibrous lesions. Most pronounced in upper lung fields.
Sxs: progressive resp. impairment.
↑risks: TB, rheumatoid arthritis, pul. HTN, rt. heart failure, lung cancer.

Front 108

Asbestosis

Back 108

Class: pneumoconiosis
Cause: inhalation of asbestos; mining, milling, insulation construction, demolition, etc.
Path: macs secrete fibrogenic/chemotactic factors. Presence of asbestos bodies. Most pronounced in lower/subpleural lung zones.
Onset: 10-20+ years of exposure.
Sx: progressive resp. impairment, pul. HTN., rt heart failure, lung cancer (usu. adenocarcinoma. Mesothileoma rare, but only assoc. with asbestos), pleural lesions.

Front 109

Hypersensitivity Pneumonitis

Back 109

Hypersensitivity to inhaled organic dust/Ags: thermophilic actinomycetes, moulds (farmer's lung), animal proteins.
Sxs: acute flu-like, or chronic from prolong low conc. exposure (dyspnea, dry cough, fatigue, malaise, eventually irreversible lung damage. Type III and IV
Path.: chronic or granulomatus interstitial pneumonia with interstitial fibrosis.

Front 110

Acetaminophen Toxicity

Back 110

Tylenol detox'd by sulfation and glucuronidation in liver by reduced GSH. Overdose depletes GSH, toxic metabolites accumulate. Massive centrolobular hepatic necrosis 3-5d after.
Tx: acetyl cysteine, or pump stomach if within 12h.
Notes: Alcohol will tie up GSH, ↓g tolerance for tylenol.

Front 111

CO Poisoning

Back 111

CO: odourless, nonirritating gas from engine exhaust, fires, heating, cigarette smoke. CO affinity for Hb 200x > than O2.

Front 112

HCN (Cyanide) Poisoning

Back 112

HCN (Hydrogen Cyanide) is rapidly absorbed via bronchia mucosa and alveoli, effects within sec/mins. Blocks cyt oxidase, diffuse cellular anoxia. Almonds?

Front 113

Mercury Poisoning

Back 113

Hg binds covalently to sulfhydryl groups, denaturing proteins and inactivating enzymes.

Front 114

Inorganic (HgCl, etc) Mercury poisoning

Back 114

Not absorbed through the skin, only inhaled as vapour.
Effects: acute: proximal tubular necrosis.
Chronic: nephritic syndrome.

Front 115

Elemental/organic Mercury Poisoning

Back 115

Absorbed across skin and BBB, causes neuronal injury/necrosis.

Front 116

Lead Poisoning

Back 116

Pb inhibits δ-aminolevulinic acid (↓haeme syn.), Na-K ATPase (↑RBC fragility), mt ox-phos (neuronal loss).
Dx: basophilic stippling of RBCs, lead lines in teeth, gums, epiphyses.
Targets: Kidneys, marrow, PNS (adults), brain (children), GI,

Front 117

Silicosis

Back 117

Class: pneumoconiosis
Cause: inhalation of silica (quartz) from mining, stonecutting, polishing, sandblasting, foundry work, ceramics.
Onset: 15-20+ exposure
Path: macs secrete fibrogenic/chemotactic factors in response, creating collagneous nodule. Nodules may coalesce into large fibrous lesions. Most pronounced in upper lung fields.
Sxs: progressive resp. impairment.
↑risks: TB, rheumatoid arthritis, pul. HTN, rt. heart failure, lung cancer.

Front 118

Asbestosis

Back 118

Class: pneumoconiosis
Cause: inhalation of asbestos; mining, milling, insulation construction, demolition, etc.
Path: macs secrete fibrogenic/chemotactic factors. Presence of asbestos bodies. Most pronounced in lower/subpleural lung zones.
Onset: 10-20+ years of exposure.
Sx: progressive resp. impairment, pul. HTN., rt heart failure, lung cancer (much higher risk with smoking), pleural lesions.

Front 119

Hypersensitivity Pneumonitis

Back 119

Hypersensitivity to inhaled organic dust/Ags: thermophilic actinomycetes, moulds (farmer's lung), animal proteins.
Sxs: acute flu-like, or chronic from prolong low conc. exposure (dyspnea, dry cough, fatigue, malaise, eventually irreversible lung damage. Type III and IV
Path.: chronic or granulomatus interstitial pneumonia with interstitial fibrosis.

Front 120

Acute Radiation Poisining effects

Back 120

Timescale: days to weeks
Cellular effects: cellular necrosis, karyorrhexis (breaking up of DNA), cytoplasmic swelling/vacuolisation.
Most affected: epithelium, parenchymal, vascular endothelial, rapidly proliferating cells.
Sxs: (transient prodromal) headache, nausea, vomiting, diarrhoea, malaise, apathy.

Front 121

Late/delyaed Radiation Poisoning Effects

Back 121

Timescale: months to years
Cellular effects: fibrosis, vascular chage, vascular sclerosis, intersitital fibrosis, atrophy of parenchymal/epithelial cells, cellular atypia, genetic damage.
Sxs: (after latency) haematopoietic, GI, CNS/cardiovascular syndrome.

Front 122

Haematopoietic Syndrome

Back 122

Dose: 2-5Gy
Latency: 1-3wks
Sxs: marrow hypoplasia/aplasia, pancytopaenia, haemorrhage, infxn.
Death: 3-6 wks

Front 123

GI Syndrome

Back 123

Dose: 5-10Gy
Latency: 1-4d
Sxs: denudation/ulceration of GI mucosa; fever, diarrhoea, fluid/electrolyte imbalance, infxn.
Death: 1-2 wks

Front 124

CNS/Cardiovascular syndrome

Back 124

Dose: 10+Gy
Latency: mins-hours
Sxs: generalised damage to BVs, massive diffuse plasma leakage, severe tissue oedema, CNS (apathy, drowsiness, ataxia, convulsions, coma), hypotension, shock, cardiovascular failure.
Death: 1-2 days.