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Acem Primary > Week 1 > Flashcards

Week 1 Flashcards

1
Q

what % of total body weight and total body of water is ICF

A

40% total body weight
2/3 total body of wawter

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2
Q

what % of total body weight and total body of water is ECF

A

20% of total body weight
1/3 of total body water

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3
Q

of ECF, what % of total body weight is interstitial fluid

A

15%

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4
Q

of ECF, what % of total body weight is plasma

A

5%

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5
Q

relative levels of K and Na and major anions in ICF

A

high in K
low in Na
phosphate and protein

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6
Q

relative levels of K and Na and major anions in ECF

A

low in K
high in Na
Cl and HCO3

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7
Q

Plasma levels of;
Na
K

A

Na 150
K 5

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8
Q

ICF levels of;
K
Na
Phosphate

A

K 160
Na 5
Phosphates 140

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9
Q

with Na/K/ATPase what is the movement of Na and K

A

3 Na out of the cell
2K into the cell

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10
Q

what is the Na/K/ATPase beta subunit

A

has no binding sites

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11
Q

what is the Na/K ATPase alpha subunit

A

intracellular subunit
binding sites for Na and ATP
extracellular binding site for K

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12
Q

Describe Ficks law

A

the magnitude of the diffusing tendency is proportional to both;
concentration gradient
cross sectional area
and is inversely proportional to the thickness of the membrane

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13
Q

Define osmolarity

A

number of osmoles per litre of solution

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14
Q

Define osmolality

A

number of osmoles per kilogram of solvent

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15
Q

what is normal plasma osmolality

A

290mOsm/l

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16
Q

define mole

A

the gram-molecular weight of a substance

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17
Q

define molecular weight

A

the ratio of the mass of one molecule of the substance to the mass of 1/12 of a carbon atom

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18
Q

what is 1 dalton

A

1/12 of the mass of a carbon atom

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19
Q

define osmole

A

unti to measure the concentration of osmotically active particles

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20
Q

hyperplasia definition

A

increase in number of cells to increase the functional capacity as a whole

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21
Q

hypertrophy definition

A

increase in mass of each cell resulting in larger overall

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22
Q

atrophy definition

A

shrinkage and loss of structure of cell
increase in autophagic vacuoles

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23
Q

metaplasia definition

A

a reversible change when one cell type is replaced by another

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24
Q

what metaplasia occurs in barrets oesophagus

A

squamous to columnar

25
effects on cell of reversible cell injury
Reduced oxidative phosphorylation –>ATP depletion–>failure of Na/K ATPase pump–> loss of cell membrane integrity –>cellular swelling Increased CA2+ intracellularly–> membrane and DNA damage Defects in protein synthesis–>cytoskeletal damage–>DNA damage Swelling of ER, loss of ribosomes, membrane blebs
26
effects on cell with irreversible cell injury
Irreversible mitochondrial injury Profound membrane disturbance and loss of integrity. Lysosomes rupture and digest cellular content, swollen mitochondria, Accumulation of reactive O2 species nuclear condensation, fading and fragmentation. Cell death
27
Morphologic features of Necrosis
Eosinophilic (pink) cells - due to loss of RNA mediated basophilia Myelin figures - the phospholipid masses that can replace cells when they necrose Cell and organelle membrane fragment Nuclear changes Autolysis Heterolysis
28
In necrosis what are the nuclear changes
Pyknosis - small dense nucleus Karyolysis -faint dissolved nucleus Karyorrhexis - broken to clumps
29
6 types of necrosis
Coagulative – architecture preserved eg MI Liquefactive – liquid viscous mass – in brain hypoxic death, post bacterial infection Caseous – white, granulomatous, no architecture – TB Gangrenous – from infection Fat necrosis – in pancreas Fibrinoid – Ag-Ab mediated
30
Physiological types of apoptosis (6)
1. Developmental involution eg thymic atrophy in children 2. Involution of hormone dependent tissues eg endometrial breakdown 3. Homeostasis in normally proliferative tissues eg intestinal crypt epithelia 4. Death after purpose finished eg neutrophils post inflammation 5. Elimination of self reactive lymphocytes 6. cell death induced by cytotoxic T cells eg virus infected
31
pathological types of apoptosis (4)
1. DNA damage eg radiation, cytotoxic drugs 2. Misfolded protein build up eg mutated genes, free radicals 3. Infections eg HIV, adenovirus 4. after duct obstruction eg pancreas, parotid
32
Apoptosis definition
organised cellular death, manifested through activation of an internal suicide program, which leads to orchestrated disassembly of cellular components, designed to eliminate unwanted cells with minimal disruption to surrounding tissue
33
Morphological features of apoptosis
cell shrinkage chormatin condensation and fragmentation cellular blebbing fragmentation of apoptopic bodies phagocytosis of apoptopic bodies lack of inflammation
34
biochemical features of apoptosis
protein cleavage by caspases protein cross linking by transgluatminase cleavage of DNA plasma membrane alterations
35
How is the Extrinsic pathway of apoptosis activated/initiated
Death receptor initiated TNF and Fas receptors on the cell surface contain a death domain
36
In Extrinsic pathway of apoptosis what activates after the death domain is initiated
Intracellular caspases particularly Caspase 8
37
In the extrinsic pathway what happens after caspase 8 is activated
caspase-8 can propagate the apoptotic signal by cleavage of further downstream effector caspases such as caspase-3. Together with other enzymes induces mitochondria to release pro-apoptotic factors such as cytochrome c resulting in the formation of the apoptosome complex
38
What happens at the start of the Intrinsic pathway of apoptosis
Mitochondrial outer membrane permeabilisation (MOMP) causes release of apoptogenic proteins such as cytochrome C, endoG, Smac/DIABLO, AIF-1, and Omi/HtrA2
39
In the Intrinsic pathway what happens after the release of cytocrome C
leads to its interaction with Apaf-1, allowing the cleavage of procaspase-9, the formation of the Apaf-1/caspase-9 apoptosome complex, and the subsequent activation of effector caspases
40
what are the 5 biochemical themes in cellular injury/death
ATP depletion Irreversible mitochondrial damage Loss of calcium homeostasis Oxygen derived free radicals Defects of membrane stability
41
How do you calculate loading dose?
Loading dose = Vd x target concentration
42
How do you calculate maintenance dose?
Dosing rate = clearance rate x target concentration Divide this my fraction of bioavailability
43
what is the henderson hesselbalch equation
pH = pKa + log 10 (A- /HA)
44
describe weak acid
weak acid gives H+ weak acid more lipid soluble at acidic pH In kidneys weak acid are excreted faster if urine is alkaline
45
describe weak base
weak base takes H+ weak bases are mor lipid soluble at alkaline pH In kidneys weak base are excreted faster if urine is acidic
46
what is EC50
EC50 is dose required for an individual to experience 50% of maximum effect
47
define ED50
ED50 is the dose for 50% of population to obtain the therapeutic effect
48
Define Zero order kinetics
the rate of elimination is constant regardless of concentration of the drug
49
Define first pass elimination
Drug metabolism in gut wall, in portal blood or most commonly hepatic clearance of drug from portal circulation prior to reaching systemic circulation
50
what are phase 1 reactions
modifications so a reactive and polar group is added to the drug. Can occur via oxidation, reduction, hydrolysis, cyclization
51
what are phase 2 reactions
conjugation. Drug is combined with charged molecules such as glucuronidation, acetyl, sulfate, glycine. This aims to detoxify and produces more polar product–> more water soluble and easier to renally excrete
52
define what a membrane potential is
electrical potential difference across a cell membrane, caused by unequal distribution of ions.
53
second messenger cAMP pathway and effects
from ATP via adenylyl cyclase (GPCR) activates PKA = protein phosphorylation
54
second messenger cGMP pathway and effects
From GTP via guanylyl cyclase activates PKG = regulars smooth muscle
55
second messenger IP3 pathway and effects
From PIP2 via PLC (GPCR) releases Ca from ER
56
second messenger DAG pathway and effects
from PIP2 via PLC activates PKC
57
second messenger Calcium pathway and effects
from ER or extracellular influx binds calmodulin
58
second messenger NO pathway and effects
diffused into cell, activates cGMP causes vasodilation

Acem Primary (18 decks)

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