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BVMS Module 4 > Week 1 > Flashcards

Week 1 Flashcards

1
Q

what is pharmacokinetics?

A 
translocation and metabolism of drugs
Absorption 
Distribution
Metabolism
Elimination

food in, exocrine secretoin, absorption, excretion.

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2
Q

describe Absorption?

A

oral, most common, can be intravenous straight to plasma
Solublity - water, lipid.
Ionisations status pKa - weak acids and weak bases.

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3
Q

what is Vd?

A

volume of plasma that would contain the total body content off the drug at the conc equal to the plasma

Vd = amount of drug in body / conc of drug in plasma

drugs with a HIGH Vd have a high conc in extravascular tissues.

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4
Q

describe metabolism?

A

Phase 1/ Phase 2 reactions.

Drug - Phase 1 - Derivative - Phase 2 - Conjugate , increase in H2O solubility as it goes on.

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5
Q

Phase 1 - describe it?

A

includes oxidation, hydrolysation, hydrolysis. derivative is made

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6
Q

Phase 2 - desicbe it and give some reactions?

A 
conjugate made 
common conjugates in cats - glucuronyl - glucorndation 
sulphate - suplhation 
methyl - methylation 
common in dogs - acetyl - acetylation.
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7
Q

Phase 1 - give some common reactions?

A 
reactions -     Locations -     enzymes 
oxidation       Liver.               Cytochrome P450
reduction.      lungs
hydrolysis       skin 
hydration.       kidney
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8
Q

what does Cytochrome P450?

A

cycle eneyxme reaction
DOGS - greyhounds deficient in subtype of P450,
can use at different doses and frequrenxyx
CATS - deficient in demethyaltion
PIGS - altred metabolic activity
RUMINANTS - plasmasoudoestrane deficiency.

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9
Q

what consequences can occurs form phase 1/2 reactions/

A

poor bioavaialbilty, larger does needed, marked inter-indivial variation, species, breed, indiviudal etc

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10
Q

what does the induction of micromomal enzymes do?

A

some drugs induce synthesis of microsomal enzymes , results in ⬆️ metabolism + increase/decrease toxicity.

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11
Q

what is clearance?

A

effieceny pf irreversible wlimatoin of a drug form the systematic circulation
OR
volume of blood cleaned of a drug per unit time.

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12
Q

what are OCTs and OATs

A

organic cation transports and organic anion transports.. passes into the gut and removes more waste products

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13
Q

what is enteroheptic circulation?

A

gut is able to breakdown molecules, glucoropides hydrolysed and reabsorbed - up to 20% of drug.

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14
Q

describe 0 order kinetics?

A

Sc/St = k

rare in practice

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15
Q

Describe 1st order kinetics?

A

Sc/St = kC

most drugs

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16
Q

what is half life?

A

amount of time taken for a quantity to fall to half it value as measured at start of time period

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17
Q

what is affinity?

A

a measure of the attraction between drug and receptor

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18
Q

what is Efficacy?

A

the ability of a ligand, once bound, to elicit a response

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19
Q

what is an agonist?

A

is a chemical that binds to a receptor and activates the receptor to produce a biological response.

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20
Q

what is an antagonist?

A

type of ligand or drug that avoids or dampens a biological reaction. Upon binding to the receptor, it does not activate.

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21
Q

what are the Types of antagonism?

A

completive and non-competitive,
physiological
chemical
pharmacokinetic

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22
Q

what is a single compartment model (Pharmacokinetic)

A

a single, well-stirred compartment into which a drug is introduced and is well eliminated

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23
Q

what is a two compartment model? (pharmacokinetics)

A

admin i.v. “central compartment
distribute to “peripheral compartment
extra compartments affect time to drug action NOT steady state

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24
Q

name the parameters used to investigate liver damage?

A

Hepatocellular enzymes

Billary enzymes.

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25
Q

name the hepatocelluler enzymes used for liver investigation?

A

Alanine aminotransferase
Asparate aminotransferae
Sorbitol dehydrogenase
Glutamate dehydrogenase

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26
Q

describe how Alanine aminotransferase is used for liver damage?

A

leaks from cytosine of damaged hepatocytes. liver specific.
small animals mainly.
there is a poor correlation between serum levels and hepatic dysfunction.

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27
Q

describe how Asparate aminotransferae is used for lover damage?

A

cytosolic + mitochondria isoenzymes exist, food in skeletal + cardiac muscle + erythrocytes.

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28
Q

desire how Sorbitol dehydrogenase + Glutamate dehydrogenase r used for liver damage?

A

both, cytosol (fluid) of hepatocytes
SDH - useful in horse and cattle
GLDH - horse and cattle, sensitive monitor for hepatic injury

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29
Q

how are Biliary enzyme used for liver damage?

A 
alkaline phosphate (ALP) 
gamma glutamyl transferrace (GGT)     = both membrane bound enzymes
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30
Q

how is Alkaline Phosphate (ALP) used for diagnosis of liver damage?

A

found in hepatocytes, impairment of bile flow, markedly increased ALP activity.
Isoenzymes, hepatic, inerrnal, bone, placental.

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31
Q

what does ⬆️ ALP indicate? in liver?

A

cholestasis, drug induction, bone remodelling
DOGS - steroid induced ALP unique in dogs
CATS - less capacity for hepatic production of ALP
L.A - wide referee ranges.

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32
Q

how is gamma glytanyl transferase (GGT) used for diagnosis of liver damage?

A

found in hepostabilty system + renal tables.
useful for cattle, horses and cats
GGT may rise in dogs - recovery costocortiods,
renal disease - GGT found in urine!

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33
Q

what parameters can be used to access hepatic function?

A

Bilirubin
Bile acids

Albumin 
Cholesterol 
Urea
Clotting factors
glucose
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34
Q

how is Bilirubin used as a parameter for hepatic function?

A

pigment produced by degeneration of heme proton of haemoglobin. RBCs lyse and heme is converted into bilirubin, is transported to liver, attracts albumin, liver takes up bilirubin it conjugates to be one water soluble and excited put bile duct of large intestine.

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35
Q

describe hyperbilibrumia?

A

pre-hepatic - haemolysis ⬆️ bilirubin , hepatic uptake, conjugation
Hepatic - anorexia/fasting in horses. may ⬇️ uptake of hepatocytes, inter-hepatic cholestasis
Post-hepatic - bile duct tumours, cholelithiasis, obstructer of bile flow.

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36
Q

what are bile acids?

A

synthesised form liver form chloerstol. used to solubuse lipids, aid fat digestion. recycled using enterohepatic circulation.

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37
Q

what is bile acid test?

A

DOGS/CATS - fasting + post prandial
2hrs later - serum bile acids measured
feeds include a bolus of bile acid to be released into intestine

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38
Q

increased bile acids effects?

A

portosystemic shunts - portal blood bypasses liver, hepatic atrophy.

Liver failure

Cholestrosis - causes relax pf bile acids in blood
bile acids not functional.

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39
Q

what is toxicology?

A

scientific discipline, overlapping with biology, chemistry, pharmacology, and medicine, that involves the study of the adverse effects of chemical substances on living organisms and the practice of diagnosing and treating exposures to toxins and toxicants.

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40
Q

what is poison?

A

substance which destroy life or injuries health when introduced to a living organism

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41
Q

what is toxicity?

A

high due or high sensitivity

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42
Q

what is LD?

A

lethal dose LP50 - dose to kill 50% test population

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43
Q

what is ED?

A

effective dose - ED50 - does to benefit 50% population

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44
Q

what are the 5 basic routes of intoxication?

A

ingestion, cularnaous, inhalation, injection, other,

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45
Q

how do you know if an animal has been treated from poison?

A

breathing, HR and temp stabilised, info form owner, prevent more poison, an antidote has been given.

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46
Q

what is gastric evacuation in an animal?

A

soon after injection - removes 40-60% ingested matter.

drugs to stimulate CTC to induce vommiting.

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47
Q

what are some products used to cause vomiting after poisoning?

A

Adsorbents - actiavted charcoal (slurry) acts as a sponge.
Give orally
Chelating agents - bind metal ion, bored ions `re chemically insert, chemical reaction, this preventing poisoning
Carthartics - sodium or magnesium sulphate - pull water into gut and increase movement though gut.

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48
Q

chocolate poison?

A

chocolate - source: theobromine occurrence: 3rd most common toxicity: white is most with milk the least. NO ANTIDOTE for it.

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49
Q

Rat poison (anticoagulant rodenticides)

A

1st gen - warfrain (less toxic)
2nd gen - difernancum (highly toxic)
occurrence: usually dogs
toxicity: vitamin K antagonist (reversible tho), interferes with clotting factors
Clinical signs - depression + anorexia, acute ingestion of very high doses = vascular collapse
Diagnosis - prodding clotting time, urine analysis, haemorrhage,
TREATMENT : vitamin K1, menadine, posit K1 (vit k3 not effective, not effective for treating rodenticide toxicity due to its delayed onset of action.)

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50
Q

Antifreeze poison?

A

attractive taste, common in cats highly mortality.
Toxicity: LD50 metabolites are toxic,
Clinical signs: weaness, vomiting, uncoordintaion, thirst, urine production, blood in urine
Treatment - Ethanol, substitute for ADH enzyme
20% ethanol IV 5.5ml/kg
5% sodium bicarbonate 8.8ml/kg counteracts acidosis caused by glycolic acid

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51
Q

what are some psychoactive drugs?

A

cocaine, amphetamine, narcotis
occurrence: little documentation but its a risk with sniffer dogs etc.
Toxicity: generally rapid CNS effects
Treatment: decontamination, specific antagonists.

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52
Q

Paracetamol poison?

A

household supplies,
occurence: rats especially susceptible
LD50 - cats 50-100 mg/kg
N-acetyl-p-benzoysime
clinical signs - facial/pulmonary oedema, cyanosis, lover damage, haemolysis, jaundice,
treatment - decontamination, supportive
N-acetyl-p-benzoysime precursor (toxbox)
Toxbox contains key treatments and antidotes.

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53
Q

what is the VPIS?

A

Veterinary poisons information service - subscription needed, not public, 12000 cases held,
provides: risk asseemsnts,, lab services, identity tablets, antidote, prefume survaalive.
provides a TOXBOX - activated charcoal - binding toxins
vit K1 - rat poison
intralipid 20%

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54
Q

what is cell injury

A

adaptive change, reversible cell injury or irreversible cell injury

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55
Q

what are the adaptive responses to normal cells?

A

⬆️ cell activity = hypertrophy / hyperplasia
⬇️ cell acvtivity = atrophy
Altered cell type = metaplasia/dyplaisa

56
Q

what are liable cells?

A 
proliferate contovery 
short life span 
high capacity to regenerate
bone marrow 
gut epithelium.
57
Q

what are stable/quiescent cells?

A

divide infrequently, can regenerate alot

58
Q

what are non-dividing cells?

A

didvid only in FOETAL life
cannot be replaced instead repair occurs
dead cells removed - matrix (collagen) fill gap
results in strength of tissue maintained but speciclaed function lost.

59
Q

what is hypertrophy?

A

increased size of organs, increased mechanical workload, stable and permanent cells

60
Q

what is hyperplasia?

A

increased size due to increased cell number, response to growth factor stimulation
can be regenerative repose to chronic tissue

61
Q

describe hypertrophy?

A

physical demand - increased workload - hormonal stimulation
pathology - increased resistance, abnormal increased in hormonal stimulant
cellular levels ⬆️, ATP⬆️, ⬆️enzyme activity, ⬆️myofilaments.

62
Q

what is Feline Hypertrophic cardiomyopathy?

A

middle aged cat males 10-20% heart failure, inherited component, affects MYOSIN BINDING PROTEIN C leading to sarcomeric disarymication.

63
Q

describe hyperthyroidism?

A

increased levels of thyroid hormone T3+T4, ⬆️adrengeric receptor - peripheral vasodilation -⬆️ HR - functional hypertrophy of heart - concentric myocardial hypertrophy.

64
Q

what is hepatocyte hypertrophy in dogs?

A

chemical drugs - ⬆️ hepatocytes - ‘enzyme induction’ - hepatocyte hypertrophy

65
Q

describe hyperplasia?

A

⬆️ cell number - response to growth factor/division - liable/stable cells - cystic endothelial hyperplasia.causes liver regeneration. TNF - IL-6 - Primises - G0-G1(mitosis) - cell proliferationtion.

66
Q

what is Atrophy?

A

decrease in cell + organ size. at cellular level - protein synthesis + increased breakdown of protein/organelles

67
Q

what in involution?

A

due to altered/decreaded hormonal stimulation - uterus post-mortem, thymus with ageing.

68
Q

Describe the pathological side of atrophy?

A

nutrient deficnciy, disuse muscle in limbs, denervation - skeletal muscle causes damage to nerves, Pressure, loss of endocrine stimulation

69
Q

what is serous atrophy of fat?

A

important finding of portmortum, suggests starvation.

70
Q

what is disuse atrophy?

A

causes shrink ness of muscles

71
Q

what is neurogenic atrophy?

A

loss of muscle mass due to nerve damage

72
Q

wha is pressure atrophy?

A

hydrocephalus - brain has collapsed due to muscle dilation chambers

73
Q

what is hypoplasia?

A

failure to aching normal size development

74
Q

describe testicular hypoplasia?

A

reduced fertility, unilateral or bilateral, testes soft + floppy.

75
Q

what is Aplasia?

A

complete lack of development -intertsial agencies, lack of connection between S.I and CI

76
Q

what is metaplasia?

A

adult cell types replaced by another adult cell type. adaptive substitution, squamous metaplasia - ciliated epithelium, possibly reversible if caught early.
causes - chronic persistence/

77
Q

what is Dysplasia?

A

disordabaly arrangement of epithil cells with - loss of differentiation, loss of cell polarity, features of atypia

78
Q

what is cell injury?

A

reversible and non-reversible(necrosis + apoptosis)

Oxygen deprivation - hypoxia and ischemia.

79
Q

what is Apoptosis cell death

A

controlled cell death, due to mechanical trauma, extreme temps, sudden changes, radiation
causes - arsenic, cyanide, air pollutants, industrial hazards, recreational drugs, therapeutic drugs.

80
Q

immunologic dysfunciton?

A

immune system - defence against infections pathogens, but immune reactions also cause cell injury

81
Q

what are some structural/biochemical targets + mechanise in cell injury?

A

mitochondrial damage = ⬇️ ATP production
entry of Ca2+ = upsets calacum balance
oxidative damage = ⬆️ROS
membrane interyriey = cell membranes
protein misfiling + degeneration. = endoplasm reticulum stress.

82
Q

what is reversible cell injury?

A

hydropic change/degeneration - acute sweating, failure of energy-depenednt ion pumps in plasma membrane. ionic fluid homoeostatis.

83
Q

what is hydopic degeneration?

A

gross exam - organs overload, pale, thyroid -
microscopic exam, cytoplasm pale.
increased H2O = organelles distingaute

84
Q

give an example of viral infection with ballon degeneration?

A

ORF (contagious ecthylumus) on muzzle crusting parapoxvirus infection, cytoplasmic inclusion in the vesicle phase.

85
Q

give some example of causes of fatty liver?

A 
increased metabolsumm of fat stores - late pregnancy
national disorders - obesity
endocrine diseases - diabetes 
1) excessive intake from gut
2) decreased B-oxidation 
3) impaired apoprotein synthesis. 
appears yellowish/pale
86
Q

describe the microscopic patterns of heptaocellular lipid vasculation?

A

macrovesicular lipidosis - single large round vacuoles filling cytoplasm - peripheral displacement of mucous, triglycerides with hydrophyism.

87
Q

what is micro vesicular lipidosis?

A

multiple small round vacuoles, indicator of more severe hepatoculler function, toxic hepatpthesis.

88
Q

describe Equine hyperlipermia?

A

highest risk when pregnant, old age
⬆️ metabolism of FA + glycerol
⬆️ hepatic synthesis of triglyceride as VLDL, insulin resistance.

89
Q

describe Feline hepatic lipidosis?

A

obese female cats, stressed with inadequate food Intale, vomit, anorexia, etc.
⬆️metabolism of non-estieraed FA

90
Q

describe excessive hepatic glycogen accumulation?

A

diabetes mellitus

glycogen accumulation in hepatocytes. - renal proximal tubule epithelium. B-CELLS of pancreatic isles of langerhans

91
Q

what is steroid hepatopathy?

A

prolonged corticosteroid/glucorticord treatment
hyperadrenocortisism resulting from - functional adrenocortical tumours - functional (ACTH) pituitary tumors, resulting in adrencortical hyper function.

92
Q

describe glucocorticoid hepatophty in dogs?

A

intratoplasmic accumulation of glycogen + fluid influx = marked hepatocelluler swelling vascoualtion, maintained numeral liver function.

93
Q

what is neurone chromoalysis ?

A

chromoatolysis of neuronal cell bodies

94
Q

what is equine grass sickness?

A

destruction of autonomic ganglia, addocaitaion with grazing, neurtogen obstruction of tract, usually fatal!

95
Q

what is irreversible cell injury?

A 
norma - reversible - irreversible
factors - severe ER swelling
- severe mitochondrial swelling
- lysosome rupture
- membrane fragmentation
- number membrane rupture
96
Q

what happens to Ca2+ in cell injry

A

increased cytosolic Ca2+ released, sources are mitchondiral, smooth ER, injuries agent.
outcomes - membrane damage, nuclear damage, ⬇️ ATP

97
Q

name the 4 ROS?

A 
O2- = superoxide anion 
H2O2 = hydrogen peroxide 
OH- = hydroxyl radical 
ONOO- = peronitrate anion
98
Q

what are free radicals?

A

reduction - oxidation reactions
absorption of radical energy
rapid burst of ROS by activated leucocytes - inflammation
transition of Fe + Cu catalyse formation of free radicals/ROS
generated by endothelial cells

99
Q

describe necrosis?

A

uncontrolled cell death, cell swells, - breakdown of plasma membrane, organelles + nucleus, leakage of contrast - neutrophils attack cells

100
Q

describe apoptosis?

A 
controlled cell death - 
condensation of chromatin
membrane blebs
cellular fragmentation
phagocytosis of apoptotic cells and fragmentation
101
Q

what is hypoxia?

A

partial reduction in oxygen conc supplied to tissues, complete oxygen deficiency = anoxic.
possible causes - heart failure, repsiatry failure, loss of blood supply (ischemia)

102
Q

what is Ischaemia?

A

partial reduction or compel loss of blood supply caused by local impairment of blood flow
blockage of blood supply, partial and venous drainage.

103
Q

what are some possible causes of ischeamia?

A

thrombosis and mechanical interference with blood flow.

104
Q

what is infarction?

A

tissue death (necrosis) due to inadequate blood supply to the affected area. It may be caused by artery blockages, rupture, mechanical compression, or vasoconstriction.

105
Q

name the different types of necrosis?

A
  1. Coagulative necrosis - ischaemia/toxic induced
  2. Liquefactive necrosis - ischaemia/toxic induced in CNS
  3. Casesous necrosis - mycobacterial infections, competent cell death, (cottage like cheese macroscopic appearance
  4. Gangerous necrosis - dry/moist/gaseous, ischaemia, bacterial toxic, (frostbite)
  5. Enzymatic necrosis - adipose tissue necrosis
106
Q

describe the morphology of cell death?

A

cytoplasmic changes - early phase - cytoplasm becomes nonogensis pink in H&E stain
increased eosinophilia - loss of RNA, consoidaiton of cytoplasmic components.
Late phase - cell rupture with loss of integrity + release of cell components.

107
Q

describe the nuclear changes involved in necrosis?

A

pyknosis - shrunken dark, homogenous round.
karyorrhexis - nuclear envelope ruptured dark nuclear removal into cytoplasm.
Karyolysis - nuclear very pale
Absence - complete dissolved or lysed.

108
Q

describe the cellular changes in necrosis?

A

normal renel tubes cells - cells with brightly eosinophilic homogenous cytoplasm - pale ghost-like cells. loss of adherence.

109
Q

name the common causes of coagulative necrosis?

A

hypoxia cell injury, local loss of blood supply, INFARCTION - necrosis due to ischaemia.

110
Q

what is renal tubular coagulative necrosis?

A 
important nephrotoxins 
plants. oak, acorn = cattle
cats - easter lily
pigs - redraft pigweed
dogs - raisins/grapes
111
Q

what is infections bovine rhinotracheitis?

A

bovine hepesvirus 1 -transient, acute, febrile illness.
severe hyperaemia + formal necrosis of nasal, pharnygeal, laranygeal
thick plague of fibreantci exudate - covered the laryngeal + trached mucosa.

112
Q

what is canine infectious hepatitis (CAV1)?

A

liver enlarged + friable will often see fibrin on capsular surface.
granular appliance to serosae
Gall bladder wall thickened by oedema.
fibrin overlies liver lobes
large basophilic intranuclear inclusions in hepatocytes.

113
Q

describe bovine tuberculosis?

A

myobacterial bovis inhaled ➡️ bacilli within alveolar spaces in lungs ➡️ phagocytoised by alveolar macrohopages ➡️ bacteria killed ➡️ infection stopped OR inhibition of macrophage bacterlaocal acitivty ➡️ macrophages killed, bacterial spread, propagation of infection.

114
Q

what is caseous lymphadenitis (CLA) in sheep/goats?

A

corynebacterium pseudotuberculosis - shearing wounds, spread by ruptured abscessed, oral or nasal secrebtum, incubation = 3 months

115
Q

what is liquefraction necrosis in CNS?

A

hypoxia or toxin induced neural necrosis ➡️ enzymatic dissolution of the neutrophil, little or absent fibrosis connective tissue in CNS.
lack of necrotic tissue support, resulting in cavity filled with fluid. debris membrane fluid cleared by macrophages.

116
Q

what is Gangrene?

A

3 types - moist, dry, gas

117
Q

describe moist Gangrene?

A

coagulative necrosis - infarction, gross findings= soft moist, brown/black, putrid smell

118
Q

describe Dry Gangrene?

A

secondary coagulation with infarction- extremites - (distal limbs, tail, ears, udder etc)
cold - frostbite.

119
Q

describe Gas gangrene?

A

anaerobic bacteria proliferate + producing toxins in tissue, bacteria intodicded by penetrating wounds into muscles
appearance - gas, bubbles.

120
Q

describe Blackleg?

A

clostridium chavvei - bacteria not introduced with wound, spores spread haemotogly from the intestine - + lodge into muscles.

121
Q

describe Fat necrosis ?

A

enzymatic - acute pancreatic necrosis/pancreatitis
tramatic - crushed fat - pelvic fat in dysteria, seemed fat of ruminant animals.
Abdominal fat is mesentery, omentum, retropartirum.

122
Q

what are some possible sequels to necrosis?

A

inflammatory reaction with visible tissue (white blood cells, hyperaemia)
digestion + liquéfaction to necrotic tissue: phagocytosis by macrophages
Regeneration of normal tissue

123
Q

explain the 2 apoptosis pathways?

A

extrinsic = death receptor pathway - receptors, Fas, TNF receptor
intrinsic - mitochondrial pathway - cell injury

both phases can switch at the INITIATOR CAPASE

124
Q

describe the intracellular accumulations?

A

excessive normal cellular component
abnormal exogenous substances
The normal cell accumulate abnormal amount of substance either for temporary or permanently which may be harmful to the cell and may cause injury

125
Q

describe the extracellular accumulations?

A

amyloid, calcification, arthritis(gout) (to much uric acid in the body)
recombinant proteins in the culture medium of Escherichia coli is desirable but difficult to obtain

126
Q

what are the causes of intracellular accumulations?

A

Decreased rate of metabolism, build up of normal endogenous substances.
Henetic or acquired defects in metabolism, packaging, transport or secretion
Failure of enzymatic marching to degenerate or transport an abnormal exogenous substrate.

127
Q

explain hepatic lipidosis?

A

normal cell ➡️ fatty liver due to abnormal metabolism
proteins mutations - protein resorption droplets, Russell bodes in plasma cells - defective protein folding - accumulation of abnormal proteins.

128
Q

what are some lysosomal storage diseases?

A

lack of enzyme - lysosomal accumulation of endogenous materials. b1 -galaclosidate + a- neuraminidase deficiency leads to intracellular accumulation (in neurones mainly)

129
Q

describe lipofuscin?

A

pigment that accumulates in post-mitotic cells, yellow-brown pigment granules composed of lipid-containing residues of lysosomal digestion. neurone and myotcytes + stable cells (hepatocytes)
indigestible - accumulates in lysosomes.

130
Q

what is haemosiderin?

A

iron-storage complex that is composed of partially digested ferritin and lysosomes. RBC breakdown, local haemosiderosis (bruising)

131
Q

name the main extracellular accumulations?

A

amyloid - diverse group of glycoproteins (B-pleatal sheet configuration,
Histolgy - eosinophilic amorphous, hyaline substance
Amyloidosis - secondary amyloidosis - to chronic inflammation/neoplasia, sustained antigenic stimulation most common in all animals
Primary amyloidosis - plasma cell tumours, rare in domestic animals

132
Q

describe renal amyloidosis?

A

globular capillary basement membrane, globular messanagium, interstitium of medulla and/or cortex,
Clinical corrections - anasarca = generates oedema ascites = serous fluid in peritoneal cavity.

133
Q

what is pathologic calcification?

A

calcium salts deposited in tissues, indicator preview ofinjury, white and gritty, calcium salts stain blue with H&E

134
Q

what is dystrophic calcification?

A

associated with necrosis,, most potent in coagulation + cases necrosis in fat necrosis.
dead/dying cells cannot regulate cytoplasmic calcium influx, calcium accumulated in mitochondria.

135
Q

describe metastatic calcification?

A

occurring in normal tissue secondary to hyper-calcium. energy of large amount of calcium ions into cells leads to calcium ions predicate on organelles.

136
Q

what are the most common cases of pathologic calcification?

A 
renal failure 
vit D toxicosis 
parathyroid hormone PTH
PTH-release protein (PTH-rp)
Destruction of bone from primary problems.

BVMS Module 4 (3 decks)

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