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124 Cards in this Set

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Fatty Change (Steatosis)
Accumulation of TGs, usu. in hepatocytes. Potentially reversible. Causes: toxins (ethanol), protein malnutrition, diabetes mellitus, obesity, overeating, hypoxia.
Atherosclerosis
Accumulation of cholesterol/CEs within sm mm and macs. (extracellular accumulations can also occur)
Spongiform Encephalopathy
A prion disease of α-helical to abnormal β-pleated sheets.
Haemosiderosis
Mild accumulation of iron (pigment) haemosiderin with no damage or impairment.
Haemochromatosis
Marked accumulation of iron pigment with damage to:
Organs: liver, pancreas, heart, skin, endocrine.
Sxs: liver dysfunction (cirrhosis), DM, ↑skin pigmentation.
1° Haemochromatosis
Genetic due to mutation in short arm of chr. 6 causing ↑ intestinal absorption.

Sxs: Cirrhosis, DM, skin pigmentation. "Bronze diabetes".
2° Haemochromatosis
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,
Dystrophic Calcification
Pathologic depositon of calcium in necrotic/damaged tissue with normal serum [Ca2+].

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

Calcification is basophilic
2° Hyperparathyroidism
Usually associated with chronic renal failure.
Multiple Myeloma (plasma cell neoplasm)
Amyloidotic disease

Precursor: Ig light chains
Major fibril: AL

Systemic manifestations
Inflammatory Amyloidosis (eg. Rheumatoid Arthritis)
Amyloidotic diseases

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

Systemic Manifestations
Alzheimer's Disease
Amyloidotic disease

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

Localised cerebral plaques
Benign Prostatic Hyperplasia
Acinar epithelial, sm mm, and stromla fibroblasts all can experience hyperplasia due to hormonal stimulation. Key histologic feature is papillary infoldings of glandular epithelium.
Ischemic/Hypoxic Cell Damage
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.
Progeria (Hutchinson-Gilford Syndrome)
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
Werner's Syndrome
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.
Acute Inflammation
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
Chronic Inflammation
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.
Granulomatous Inflammation
Special form of chronic inflammation.
Causes: TB, Histoplasma capsulatum, sutures, lipids.
Features: Caseation often seen in centre, surrounded by epithelioid macs, surrounded by lymphocytes.
Pitting Oedema
Caused by ↓'d plasma oncotic pressure from ↓'d albumin syn.; indicative of liver dysfunction.
Ehler-Danlos Syndrome,
Osteogenesis Imperfecta
Diseases of collagen malformation
Marfan Syndrome
Defect: Fibrillin (component of elastic fibres)
Pulmonary Oedema
A potentially fatal form of odema which impairs resp.
Brain Oedema
Potentially fatal odema; swelling withing confined skull leads to herniation, impairment of blood flow, and disruption of brain stem.
Congestive Heart Failure
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.
Left-sided Failure
Results in pulmonary congestion/oedema and ↓'d renal perfusion. Leads to prerenal azotaemia (↓'d protein excretion), activation of reinin-ATN-aldo sys.
Right-sided Failure
Systemic/portal venous congestion, causing impairment of liver fxn.
Haematoma
accumulated blood within a tissue or space
Petechiae
Minute haemorrhages (1-2mm)
Purpura
Medium-sized haemorrhages (≤1cm)
Ecchymoses
Large, blotchy haemorrhage
Haemothorax
haemorrhage into pleural cavity
Haemopericardium
Haemorrhage into pericardial sac; will crowd the heart, preventing proper pumping (CHF)
Haemoperitoneum
Haemorrhage into peritoneal cavity
Haemoarthrosis
Haemorrhage into joint space.
Contusion (bruise)
Haemorrhage within tissue following rupture of small BV by blunt trauma.
Hypovolaemic shock
Shock due to excessive fluid loss/haemorrhage.
Cardiogenic shock
shock due to ↓'d C.O.
Neurogenic shock
shock due to deranged peripheral vasomotor control from NS injury. Mechanism similar to shock caused by sepsis, drugs, and anaphylaxis.
Septic Shock
Usu. due to gram neg bacilli endotoxin (LPS), causing 2° release of vasodilating and pro-coagulating cytokines
Acute Tubular Necrosis
Renal manifestation of decompensated shock.
Centrolobular Necrosis
Hepatic manifestation of decompensated shock, because that's where the blood is most deoxygenated.
filariasis
parasitic worm that enters and blocks lymph vessel, causing localised oedema.
Classic Haemophilia (Haemophilia A)
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.
Christmas Disease (Haemophilia B)
Factor IX deficiency (intrinsic pathway)
Thrombophilia
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.
Cri du chat syndrome
(5p- syndrome)
Sxs: mental retardation, developmental abnormalities.
13q- syndrome
↑'d susceptibility to neoplasm retinoblastoma, etc. Two-hit hypothesis.
Subtelomeric deletion/rearrangement
seen in some cases of mental retardation with dysmorphic features. Assayed with FISH or CGH (comparative genomic hybridisation)
Burkett's Lymphoma
Transcriptionally active gene gets translocated next to oncogene. Same mechanism as Chronic Myelocytic Leukaemia.
Turner Syndrome
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.
Down Syndrome
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.
Klinefelter's Syndrome
47XXY
Sxs: weak facial hair, gynectomastia, female fat distr., infertility, long legs, hyalinised tubules.
↑risks: breast cancer.
Cystic Fibrosis
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.
Gaucher Disease
Class: Sphingolipidosis Single base mut. in β-glucosidase. Glucosylceramide accumulates in mac lysosomes.
Dx: foamy spleen cells
Sxs: splenomegaly, anaemia, leukopaenia, thrombocytopaenia.
Type 1 Gaucher Disease
Adult onset, most common. Normal lifespan. Bone involvement can lead to disability. Suppl. with I.V. acid glucose cerebrosidase possible but expensive.
Type 2 Gaucher Disease
Childhood onset, rapid deterioration, most die before year 1.
Sxs: hepatosplenomegaly and neurological abnormalities.
Type 3 Gaucher Disease
Similar to Type 2 with neurological deterioration, but slower progression.
Phenylketonuria (PKU)
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.
Neurofibromatosis-1 aka von Recklinghausen Disease
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.
Polycystic Kidney Disease
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.
Duchenne Muscular Dystrophy
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
Fragile X Syndrome
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
Kearns-Sayre Syndrome
Mitochondrial disorder
MELAS
Mitochondrial disorder; "Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes".
MERRF
"Myoclonic epilepsy with ragged-red fibres"; a mitochondrial disease.
Leber Hereditary Optic Neuropathy
Mitchondrial disorder
Prader-Willi Syndrome
Defect: del on paternal chr. 15q11-13, subsequent inactivating methylation of maternal copy.

Sxs: hypotonia, obesity, hypogonadism, mental retardation
Angelman Syndrome
Defect: del of maternal 15q11-13, subsequent inactivating methylation of paternal copy.
Sxs: hyperactivity, inapproriate laughter, severe mental retardation.
Kwashiorkor
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.
Marasmus
aka starvation, general deficiency of calories.
Sxs: stunted growth, loss of subcutaneous fat, atrophy of mm, prematurely aged appearancce.
Cachexia
Class: 2° protein-energy malnutrition; seen in cancer, AIDS, post-op. "Wasting away".
Anorexia Nervosa
self-imposed starvation (cf. marasmus), esp. in young women.
Sxs: amenorrhea, ↓TH, anaemia, lymphopaenia, hypoalbuminaemia, hypokalemia (↑risk cardiac arrythmia)
Vitamin A deficiency
2°: fat malabsorption.
Sxs: Night blindness, epithelial abnormalities (squamous metaplasias, keratomalacia [corneal softening], xerophthalmia[dry eyes]), ↑risk childhood infxns
Scurvy
Vitamin C deficiency
Sxs: (All related to collagen malsynthesis)haemorrhages, subperiosteal haematomas, sk changes, impaired wound healing.
Vitamin E deficiency
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.
Wet Beriberi
Thiamine (B1) deficiency
Alcoholics, gastric bypass pts.
Sxs: Cardiac sxs; may have oedema, myofibre swelling, and ind. myocyte necrosis.
Dry Beriberi
Thiamine (B1) deficiency
Sxs: Peripheral nn sxs; symmetric polyneuropathy in feet and lower legs. Spreads proximally over time. Demyelination, axonal disruption (in severe cases)
Wernicke-Korsakoff Syndrome
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.
Iron Deficiency
Causes: heavy menstrual flow, internal/GI haemorrhage, kids fed only milk after 6 months
Assoc.: hypochromic microcytic anaemia. Brain/developmental abnormalities in children.
Zinc Deficiency
Cause: usu. unsupplemented TPN, or congenital metal ion transporter deficiency.
Sxs: skin rash (acrodermatitis enteropathica), growth retardation, infertility
Selenium Deficiency
Cause: usu. unsupplemented TPN
Assoc.: congestive cardiomyopathy
Iodine Deficiency
Sxs: hypothyroidism, goiter. Iodine deficient mother can give birth to child with congenital hypothyroidism, progressing to cretinism (retardation)
Metabolic Syndrome
"Syndrome X", consisting of insulin resistence, dyslipidaemia, HTN, abdominal obesity, proinflammatory state (due to fatty liver?), prothrombotic state.
Nonalcoholic steatohepatitis (NASH)
fatty change in liver assoc. with Type II diabetes. May progress to cirrhosis.
Obesity
BMI ≥ 30
↑risk: metabolic syndrome, NASH, cholelithiasis (gallstones), osteoarthritis, lower back pain, ischaemic stroke, venous thrombosis.
Copper Deficiency
Cause: rare; usu. with TPN.
Sxs: anaemia, poor wound healing, mm weakness
Benign Neoplasm
1.) pushing, not invading borders.
2.) No metastasis
3.) Closely resembles tissue of origin
Malignant Neoplasm
1.) Infiltrating, invading borders
2.) Metastisis to distant sites
3.) Can resemble tissue of origin, or be poorly/undifferentiated (pleomorphism)
Chronic Myelocytic Leukaemia (CML)
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
CML - chronic phase
Phase I of CML; ↑ leukocyte, platelet count, <10% myeloblasts; bone marrow hypercellular, dominated by myeloid cells.
CML - accelerated phase
Phase II of CML: ≤20% myeloblasts, ≤basophils, splenomegaly, rising white count unresponsive to therapy.
CML - blast phase
Phase III (final) of CML: ≥20% myeloblasts, extramedullary deposits of leukaemic blasts, resembles acute leukaemia, poor prognosis.
Hereditary Nonpolyposis Colon Cancer (HNPCC)
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.
Familial Adenomatus Polyposis (FAP)
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.
Xeroderma Pigmentosum
Autosomal recessive with defect in nucleotide excision repair of pyrimidine dimers due to UV damage.
Malignancy
Sxs: anorexia, wt. loss, fever (TNF-α, IL-1, IFN-γ), distant effects (paraneoplastic syndromes)
Cushing Syndrome
Paraneoplastic syndrome of small cell carcinoma of lung, and carcinoid tumours.
Acetaminophen Toxicity
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.
CO Poisoning
CO: odourless, nonirritating gas from engine exhaust, fires, heating, cigarette smoke. CO affinity for Hb 200x > than O2.
HCN (Cyanide) Poisoning
HCN (Hydrogen Cyanide) is rapidly absorbed via bronchia mucosa and alveoli, effects within sec/mins. Blocks cyt oxidase, diffuse cellular anoxia. Almonds?
Mercury Poisoning
Hg binds covalently to sulfhydryl groups, denaturing proteins and inactivating enzymes.
Inorganic (HgCl, etc) Mercury poisoning
Not absorbed through the skin, only inhaled as vapour.
Effects: acute: proximal tubular necrosis.
Chronic: nephritic syndrome.
Elemental/organic Mercury Poisoning
Absorbed across skin and BBB, causes neuronal injury/necrosis.
Lead Poisoning
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,
Silicosis
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.
Asbestosis
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.
Hypersensitivity Pneumonitis
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.
Acetaminophen Toxicity
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.
CO Poisoning
CO: odourless, nonirritating gas from engine exhaust, fires, heating, cigarette smoke. CO affinity for Hb 200x > than O2.
HCN (Cyanide) Poisoning
HCN (Hydrogen Cyanide) is rapidly absorbed via bronchia mucosa and alveoli, effects within sec/mins. Blocks cyt oxidase, diffuse cellular anoxia. Almonds?
Mercury Poisoning
Hg binds covalently to sulfhydryl groups, denaturing proteins and inactivating enzymes.
Inorganic (HgCl, etc) Mercury poisoning
Not absorbed through the skin, only inhaled as vapour.
Effects: acute: proximal tubular necrosis.
Chronic: nephritic syndrome.
Elemental/organic Mercury Poisoning
Absorbed across skin and BBB, causes neuronal injury/necrosis.
Lead Poisoning
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,
Silicosis
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.
Asbestosis
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.
Hypersensitivity Pneumonitis
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.
Acute Radiation Poisining effects
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.
Late/delyaed Radiation Poisoning Effects
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.
Haematopoietic Syndrome
Dose: 2-5Gy
Latency: 1-3wks
Sxs: marrow hypoplasia/aplasia, pancytopaenia, haemorrhage, infxn.
Death: 3-6 wks
GI Syndrome
Dose: 5-10Gy
Latency: 1-4d
Sxs: denudation/ulceration of GI mucosa; fever, diarrhoea, fluid/electrolyte imbalance, infxn.
Death: 1-2 wks
CNS/Cardiovascular syndrome
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.