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Blood and Circulation > 1 > Flashcards

1 Flashcards

1
Q

where are the kidneys located?

A

posterior to the peritoneum in the abdominal cavity

the left kidney is slightly higher than the right

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2
Q

function of the kidney

A

homeostasis

blood ionic composition
blood pH (7.38-7.42)
blood volume and pressure
blood osmolarity (conc. of solutes)
excretion of waste
hormone production - locally or long distance
glucose levels - dip test on urine
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3
Q

hypovolaemia

A

blood fluid volume too little so dehydrated

thirst, postural hypotension (dizzy), low jugular venous pulse/pressure (JVP), weight loss, dry mucous membranes, reduced skin turgor, reduced urine

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4
Q

hypervolaemia

A

too much blood fluid volume

oedema (tissue swell), breathlessness, raised JVP, weight gain, hypertension

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5
Q

what contributes to blood pressure?

A

sodium and water

water follows sodium

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6
Q

interstitial fluid

A

surrounding capillaries

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7
Q

intracellular fluid

A

in cells

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8
Q

extracellular fluid

A

vasculature and interstitial fluid so in blood and around tissues

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9
Q

osmolarity

A

number of active solutes in fluid

osmoles (osmol/L, Osm/L, mOsm/L)

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10
Q

osmolality

A

like osmolarity but per kg instead of L so weight not volume

but can interchange the words

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11
Q

osmotic pressure

A

pressure applied to prevent inward fluid movement across semi-permeable membrane

high osmotic pressure means high osmolarity

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12
Q

oncotic pressure

A

osmotic pressure exerted by proteins in plasma which attract water

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13
Q

hydrostatic pressures (P)

A

force exerted by fluid against capillary wall

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14
Q

tonicity

A

effective (relative) osmotic pressure gradient, relative concentration of solutes dissolved, diff tonicities of compartments to allow movemet

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15
Q

hypotonic solution

A

high osmotic in cell
low in interstitial fluid

water moves hypo to hyper so into cell

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16
Q

isotonic solution

A

high in cell and fluid so no net movement but freely back and forth

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17
Q

hypertonic solution

A

high osmotic in cell but very high in fluid so water move out cells to fluid (from high water to low water)

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18
Q

what movement occurs if Pc (hydrostatic pressure of capillaries) is bigger than osmotic pressure?

A

fluid leaves capillary - filtration of plasma

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19
Q

diameter affects P

A

high P from large diameter e.g. large diameter of afferent arteriole and small diameter of efferent so filtrates water out capillary

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20
Q

2 different lengths of nephron

A

cortical - shorter less important

juxtamedullary - focus on this, role in conc.

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21
Q

function of nephron

A

filtration
tubular reabsorption
tubular secretion
urine excretion

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22
Q

mesangial cells

A

around afferent arteriole and vasculature

smooth muscle cells so affect diameter and surface area of filtration so change P

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23
Q

parietal outer layer of Bowman’s capsule

A

squamous cells

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24
Q

podocytes of visceral layer of Bowman’s capsule

A

fingers make another filtration layer

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25
Q

macula densa

A

wall of ascending limb

cells act as chemoreceptors to detect sodium chloride in filtrate

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26
Q

juxtaglomerular cells

A

wall of afferent arteriole

mechanoreceptors detect stretch in capillary walls

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27
Q

3 main layers for glomerular filtration

A

fenestration (pores) prevent filtration of RBCs and platelets

basal lamina (basement membrane) prevent large proteins, -vely charged

pedicels - filtration slits (allow less than 0.006-0.007um, water, glucose, vitamins, ammonia, urea)

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28
Q

NFP (details on paper notes lecture 1-2)

A

net filtration pressure
total P that promotes filtration

= GBHP-CHP-BCOP

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29
Q

GFR

A

glomerular filtration rate

amount filtrate formed per min

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30
Q

control of GFR

A

renal autoregulation - myogenic and tubuloglomerular feedback

neuronal regulation

hormonal regulation

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31
Q

renal autoregulation (myogenic and tubuloglomerular)

A

maintain constant renal blood flow and GFR

myogenic mechanism: increases BP and GFR means BP stretches walls of afferent A which is detected by JG cells so smooth muscle fibres contract and narrow lumen of afferent so reduces renal flow and GFR

tubuloglomerular feedback: -ve feedback by macula densa cells, increased filtration rate sensed by macula densa from solutes and JGA so decrease NO release (vasodilator) so afferent constrict and decrease blood flow and GFR

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32
Q

change water levels in nephron

A

most reabsorbed in PCT and Loop of Henle
fine tuning in LoH and collecting duct

thick ascending limb is impermeable to water

countercurrent system in LoH keeps gradient

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33
Q

how is glucose reabsorbed from PCT?

A 
through SGLTs (sodium glucose transporters)
so cotransported with Na

normally all reabsorbed by PCT

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34
Q

sodium ions at PCT

A

Na/H antiporter gets H into tubule to get rid of it and helps buffering, and Na out

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35
Q

ions and urea in PCT

A

passive reabsorption in distal part of PCT

leaky cells so pericellular movement and transcellular in leak channels

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36
Q

Loop of Henle absorption and secretions

A

thick ascending limb with Na/K/Cl symporters in apical membrane

potassium pumped out
chloride leaks out

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37
Q

distal convoluted tubule and collecting duct function

A

fine tuning depending on what body needs

water affected by ADH

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38
Q

what causes ADH release?

A

cellular dehydration causes increase plasma osmolarity which triggers osmoreceptors in hypothalamus
OR
extracellular dehydration decreases fluid volume and causes hypovolaemia detected by pressure sensors in peripheral volume receptors in atria/carotid sinuses/aortic arch/afferent arteriole

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39
Q

where is ADH produced?

A

supraoptic and paraventricular nuclei of hypothalamus

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40
Q

where is ADH released?

A

posterior lobe pituitary

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41
Q

mechanisms of ADH

A

vasopressin receptor for ADH on collecting duct activates PKA so phosphorylation of proteins and AQP2 export to apical membrane of cell so inserts aquaporins so water absorbed to blood

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42
Q

what is the point of the countercurrent multiplier in the Loop of Henle?

A

to increase osmotic gradient in medullary interstitial fluid

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43
Q

how does the countercurrent multiplier in the Loop of Henle work?

A

hairpin arrangement

symporters in thick AL transport Na and Cl into medulla

continued movement through tubules supplies ion for this

thin DL permeable to water and no active reabsorption/secretion occurs, water moves out due to high conc. ions in medulla

thin AL impermeable to water and no active movement of solutes

thick AL impermeable to water but active reabsorption

ions pumped out on right so water from left comes out and concentrated fluid flows from left to right in tube so high concentration on right again and pumped out again etc.

only pump out difference of 200

urea helps with gradient as well

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44
Q

renin-angiotensin-aldosterone system

A

low blood pressure/volume causes afferent arteriole to be less stretched so JGA secrete renin enzyme which causes angiotensin II (vasoconstrictor) release

so lower GFR and more Na/Cl reabsorption and adrenal cortex releases aldosterone which acts on kidneys to reabsorb water and Na so increase BP/volume

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45
Q

how is angiotensin II made?

A

angiotensinogen made by liver makes angiotensin I + ACE (angiotensin converting enzyme) which converts it to angiotensin II and acts on adrenal cortex

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46
Q

where is ACE produced

A

from renal and lung epithelia

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47
Q

ACE inhibitors

A

hypertension drugs, stop vasoconstriction, stop high BP

e.g. benazepril, captopril (more on lecture 1-2 slide 48)

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48
Q

diuretics

A

promote loss of Na and water

loop diuretics most powerful and inhibit medullar gradient

thiazide diuretics act on DCT and reduce Na reabsorption

Spironolactone - aldosterone receptor antagonist, acts because K in urine from aldosterone tubular secretion into late DCT/CT

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49
Q

atherosclerosis

A

precursor of all CVD (cardiovascular disease) apart from rheumatic

plaques
reduced lumen
reduced elasticity of vessels
clots

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50
Q

normal BP

A

120/70 or 80

120 is systolic P in artery when ventricle contract
70/80 is diastolic P

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51
Q

lipid transport in body

A

insoluble so require specific transport

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52
Q

apolipoproteins and lipoproteins definition and types

A

apolipoproteins bind lipids to form lipoproteins - 1 layer lipid membrane with proteins inside, acts as receptor

e.g. chylomicrons, VLDL (very low density lipids), IDL (intermediate), LDL, HDL (high), Lipoprotein A

(more dense means more protein)

diff densities transport diff things

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53
Q

relationships between lipoproteins and CVD

A

positive relationship between LDL-C and CVD

inverse relationship between HDL-C and CVD

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54
Q

what does LDL transport

A

cholesterol to tissues

similar to lipoprotein A but A has extra protein on outside

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55
Q

lipoprotein mechanism and function

A

chylomicron picks of triglyceride (TG) from diet to transport to liver, skeletal muscle, adipose tissue for energy or storage so smaller chylomicron remnant

VLDL made in liver carries new TG from liver to tissues so becomes IDL then LDL

2 variations: LP (a) and SD-LDL (high cholesterol and high VD)

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56
Q

chylomicron structure

A

phospholipids on outside with TG and cholesterol ester (makes more soluble) inside with proteins in phospholipid layer

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57
Q

which lipoprotein is good and reduces CVD?

A

HDL (high) because picks up cholesterol and gets rid of it

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58
Q

exogenous lipid transport pathway (how fat in diet is metabolised)

A

bile emulsify dietary fat - broken to glycerol and fatty acids

1) enterocytes package TG to chylomicron
2) through lymphatics to vasculature
3) chylomicron pick up TGs, C-II (2) on chylomicron interacts with lipid protein lipase (LPL, given off by HDL to help chylomicron bind and endocytosis) in vasculature so breaks TG to free fatty acids (FFA) and glycerol
4) offload into tissues and use FFA for metabolism
5) remnant circulates to liver where ApoE protein bind receptor in liver so broken

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59
Q

enterocytes

A

intestinal absorptive cells in lining of gut

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60
Q

endogenous lipid transport pathway

stuff made in liver

A

1) liver can generate all the cholesterol it needs
2) cholesterol packaged into LDL (HDL helps transfer Apo C-II and ApoE to VLDL)
3) VLDL binds with ApoC-II to vasculature walls and LPL breaks TG to FFA and offloads TGs
4) now IDL which turns to HDL to LDL (or straight to LDL, low density) and can bind tissues to offload cholesterol/TG
5) bind to liver by rLDL (receptor) and offload cholesterol to cells
6) lots LDL means saturate tissues and liver, reduce receptors so leave high plasma LDL (in blood) and blood LDL conc increases

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61
Q

reverse cholesterol transport

A

by HDL - when it interacts with tissues it collects cholesterol (which is good) unlike LDL which offloads it

it takes it to adrenal/ovaries/testes for steroidogenesis

can go back to liver for breakdown - receptor mediated endocytosis

talks to LDL and VLDL to offload cholesterol/proteins
so can give proteins to help other lipoproteins do job

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62
Q

atherosclerosis pathogeneis

A

high plasma level of LDL so plaques - deposition of lipids in medium/large arteries

proliferation of extracellular matrix (ECM) beneath smooth muscle layer so protrusion of fibrous plaque to lumen of vessel and affects flow

can be asymptomatic until ischaemia, closure of vasculature by plaque closure, clot, aneurysm, embolism

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63
Q

ischaemia

A

reduced O2 to tissues

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64
Q

aneurysm

A

weak walls can split

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65
Q

embolism

A

clot travel to other parts of body

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66
Q

hypotheses for atherosclerosis

A

lipid hypothesis - excess lipids

response to injury hypothesis - damage to epithelium

inflammation hypothesis - combination of both

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67
Q

neoplasia

A

proliferation of smooth muscle cells

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68
Q

prostaglandins

A

prostacyclin and thromboxane imbalance - influence thrombus formation

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69
Q

thrombosis

A

main event forming atheromatous plaques

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70
Q

stages of atherosclerosis and how it’s caused

A

1) damage endothelial cells activates cascade so inflammation and attracts WBCs

2) macrophages try take things up but can’t do anything with it so now foam cell - cholesterol becomes oxidised and more reactive to cells so more inflammation and protrusion under endothelial - fatty streak,
more ECM and plaque, compression of smooth muscle cells and cells migrate to fatty streak

3) protrusion with hard lipid core - mitochondria dysfunction, necrosis and neoplasia, epithelial cells take up lipids and lots ECM produced and proteases produced so protrusion into vasculature and it affects blood flow,
increased cell adhesion expression so sticky and platelets stick to walls so clot

4) fibrous cap, lots fibrin, lipid core, destroy underlying layer, lots collagen, more MMPs which break ECM down and make unstable which is dangerous, develop thrombus and high stage atherosclerosis

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71
Q

what causes damage to endothelial cells?

A

smoking
high BP
high lipid

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72
Q

what determines if a plaque is vulnerable?

A

composition (not size)

large lipid core more likely to rupture and expose thrombogenic material

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73
Q

treatment of atherosclerosis

A 
lifestyle change
ACE inhibitors
statins
antiplatelets for thrombus
surgery for coronary arteries and carotid arteries
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74
Q

statins

A

reduce cholesterol
stop cascade of production

Atorvastatin is common

risk of diabetes but worth the low 9% risk

60-70% CVD still not prevented

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75
Q

haemotology

A

study of blood

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76
Q

haematopoiesis

A

differentiation into all blood cells

expression of diff genes, controlled by env. of developing blood cell

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77
Q

cells in blood

A

leukocytes -white
erythrocytes -red
thrombocytes - platelets

rarely others like foetal and cancer

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78
Q

what is plasma made up of?

A 
water
electrolytes
dissolved gases
urea
proteins
lipids
glucose
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79
Q

anti-coagulated - slow centrifugation of blood

A

shows main components
buffy coat layer with WBCs
haematocrit value is % volume (roughly 45%) of RBCs

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80
Q

blood cell lineages

A

all from single pluripotent stem cells called progenitor (stem cell but more specific)

which splits to myeloid from bone marrow - platelets , RBCs, myeloblast to granulocytes (eosinophil, basophil, neutrophil)
OR
lymphoid from lymph - lymphoblast to B lymphocyte/T/natural killer

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81
Q

leukocytes (WBCs) are which lineage?

A

all lymphoid and granulocytes from myeloid

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82
Q

properties of erythrocytes

A

membrane can deform to squeeze through 3um vessel,

shape maintained by cytoskeletal system and allows flexibility

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83
Q

anaemia

A

too few RBCs

breathlessness, fatigue

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84
Q

polycythaemia

A

too many RBCs
raised viscosity
strain on heart so need to work lots

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85
Q

where are leukocytes produced from?

A

primary lymphoid tissues - bone marrow or thymus

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86
Q

where do leukocytes function?

A

secondary lymphoid tissues - spleen, lymph nodes, mucosa-associated lymphoid tissues (MALT e.g. Peyer’s patches in gut)

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87
Q

which is the most abundant WBC in blood?

A

lymphocyte and neutrophils

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88
Q

lymphocyte structure

A

25% of blood

small, same size as RBC, 1 massive nucleus fills cell

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89
Q

neutrophil structure

A

65% of blood
1.5 x RBC
multilobed

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90
Q

monocyte

A

5% of blood
kidney shaped nuclei
largest cell - 2x RBC

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91
Q

eosinophil

A 
5% of blood
same size as neutrophil
pink not blue
bi-lobed nucleus
lots granules
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92
Q

basophil

A

1% of blood
large granules
can barely see nucleus but bi-lobed
block clotting

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93
Q

which immunity corresponds to which blood cell lineage?

A

lymphocytes are for adaptive immunity - B/T/NK

myeloid lineage are for innate immunity - N/M/E/B

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94
Q

haematoxylin and eosin (H&E) stain

A

most common stain for blood

eosin is pink acidic dye which binds proteins and stains cytoplasm pink

haematoxylin is blue-purple basic dye which binds nucleic acids

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95
Q

what are platelets

A

fragments on cells NOT cells

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96
Q

histochemistry

A

stain enzymes on surface e.g. non-specific esterases turn brown

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97
Q

immunological detection

A

antibody binding of extra/intracellular AG on WBCs

immunocytochemistry - Ab linked to fluorescent chromophores, visualise on microscope

immunohistochemistry - Ab linked to enzymes to convert substrates

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98
Q

flow cytometry

A

diff coloured cells counted
intensity of fluorescence measured - dot plots (1 dot is 1 cell)
so add Ab coloured for each cell and use lasers and gate open depending on colour and counted as go through gate

lineage markers allow gate counting

99
Q

monocyte markers

A

CD14+ marker

can be detected with Ab so tells us what they are

100
Q

thrombocytes

A

platelets

formed from megakaryocyte in bone marrow,
cell attach where blood vessel is forming, project membrane through holes in vessel, bits come off to make platelets

101
Q

satellistism

A

reduced platelets

102
Q

plasma

A

fluid component of blood, with lots proteins

103
Q

plasma proteins

A

albumin
alpha globulins 1/2
beta globulins
gamma globulins

104
Q

where are plasma proteins synthesised?

A

all except gamma are synthesised by liver

105
Q

serum

A

fluid left after blood has clotted, contains all proteins except for things involved in clotting (clotting factors, fibrinogens)

106
Q

unusual results seen in gamma globulin in electrophoresis of plasma proteins

A

1 class of gamma globulin clear band instead of normal diffuse band - could be myeloma

no gamma could be leukaemia

normally diffuse band because lots diff Abs

107
Q

polypeptide hormones in blood

A

e. g. anterior pituitary secretes prolactin which acts on mammary gland and regulates blood pressure
e. g. renin and angiotensins for BP

other enzymes

108
Q

albumin

A

carrier for substances with low solubility in plasma like lipids, hormones, fatty acids

low affinity for lipophilic compounds

diminish binding of xenobiotics to hormone/receptor so protect endocrine disruption

binds calcium, helps maintain osmolarity of blood

109
Q

function of complement in blood

A

opsonisation
chemotaxis
lysis
clumping of antigen bearing agents

110
Q

gamma globulins

A

serum Abs

111
Q

alpha-antitrypsin

A

inhibit trypsin

112
Q

haptoglobulin

A

binds free Hb

113
Q

coagulation factors

A

when activated they form an enzyme cascade - convert fibrinogen to fibrin which is insoluble so trap cellular components and clot

114
Q

haemostasis

A

maintain blood fluid within circulatory system

by vasoconstriction
platelet activation
haemostatic plug
coagulation
clot
clot dissolution
115
Q

vWF

A

van Willebrand factor in endothelial

not visible normally until breakage

116
Q

haemostasis and coagulation process (clotting)

A

1) extrinsic damage to endothelium
2) platelet membrane integrins mediate adherence to ECM (integrin a2b1 binds collagen, integrin alpha2b beta3 aka glycoprotein GPIIA/III binds other ECM proteins)
3) vWF becomes visible when bound to GP1b integrin - when breakage occurs
4) platelets activated so sticky so bind vWF and collagen and to site of injury
5) prothrombin to thrombin to fibrinogen to fibrin which binds more integrins and platelets
6) binding of integrins causes activation of platelets which release ADP - signals to more platelets to clot, and platelets also release thromboxin A2 (TXA2) which activates platelets and vasoconstriction
7) activated platelets bind and release protein factors (coagulation factors, growth factors for healing) and phosphollipids up-regulated on platelets
8) tissue factor (factor II/thromboplastin) activates plasma coagulation - in tissue not circulation so clots if contact tissue

117
Q

how to prevent excessive clotting

A

thrombomodulin on endothelium binds thrombin to activate protein C so inactivate factors Va and VIIa

antithrombin in plasma

protease ADAMTS13 degrades vWF

118
Q

how to remove clots

A

fibrinolytic mechanisms
depends on fibrin digestion by plasmin protease

inactive precursor plasminogen activated by tPA (tissue plasminogen activator) to plasmin - drugs can activate this

119
Q

haematopoietic stem cell

A

blood cells constantly made in bone marrow (5 x 10^11 daily) because most blood cells short 1/2 life

accelerated when haematological stress (infection needs leukocytes, high altitude needs RBCs)

120
Q

haematopoiesis process

A

1) early in embryonic development (3 weeks in humans), not in bone marrow, embryo separate into 2 (embryo proper & adult tissues AND yolk sac)
2) yolk sac - heart forms earliest, YS joined to embryo by stalk which forms capillary system (plexus)
3) heart and aorta form same time and join with capillary plexus, RBCs start to circulate, 3 niches of RBCs are YS/liver/bone marrow

4) primitive = early haematopoiesis in YS, nuclei blood cells,
definitive = switch to liver haematopoiesis at 5 wks then BM at birth

5) bone marrow is highly specialised tissue with lots cells
6) IS cells proliferate and differentiate in periphery (2nd lymphoid)

121
Q

where are blood cells made before and after birth?

A

in development, in yolk sac and liver then switch to bone marrow at birth

122
Q

stalk that joins yolk sac to embryo

A

contains mesoderm derived stem cells - haemangioblasts which differentiate to RBCs with nuclei and endothelial cells to generate capillary system (plexus) in yolk sac

123
Q

cells other than blood cells in bone marrow

A

stromal cells for support

growth factors

osteoblasts

124
Q

bone structure

A

specialised connective tissue with rigid ECM, rigid outer layer of dense compact bone, inner core less dense spongy bone

125
Q

units of bone

A

osteon

126
Q

Haversian canal

Volkmann’s canal

A

vessels and nerves go up and down

sideways join Habersians

127
Q

bone marrow structure

A

within medullary cavity and spongy bone

2 kinds: red and yellow

red in flat bones and epiphyses of long bones, contained granulocytes, erythroid islands, megakaryocytes,
yellow in shafts of long bones (lots fat)

128
Q

Hayflick limit

A

stem cells divide certain number of times because of telomere shortening

129
Q

model explaining telomere reduction in serial transplantation

A

HSC in adult mice non stressed resting state - not much shortening

transplant to primary recipient - cycling activity increased for reconstruction of lineages

primary to 2nd recipient - considerable increase in HSC turnover so cycling time speeds, cell cycle time decreases so telomere shorten

130
Q

experiment showing HSC are multipotent

A

so parental cell for all blood cells

x-rays cause double stranded breaks in BM cells’ DNA, try repair and cause chromosome markers - each unique, so all descendents of marked cell have same marker so can map DNA mutation

found that all leukocytes had same marker, then all myeloid had same and all lymphoid has a different same marker

so stem cells more restricted potency - myeloid/lymphoid from progenitor - CLP/CMP make lymphoid/myeloid

131
Q

HSC marker (Hematopoietic Stem Cell)

A

rare cell in bone marrow (<0.1%) with CD34+ marker

but endothelial express CD34 as well so not unique to HSC

132
Q

stem cell niche for HSC

A

2 speeds of cell division

1) endosteum - long term, maintain vascular niche, between solid bone and marrow, associated with osteoblasts, SLOW cycling
2) perivascular - progenitor cells produced, region around vascular sinusoids with large vessels thin walls and fenestrated endothelium, FASTER cycling

receptors on niche and HSC so bind and signal to each other

133
Q

stem cell niche (definition + 3 types)

A

microenvironment around stem cells provide support and signals regulating self-renewal and differentiation

1) direct contact: physical, juxtacrine, stem cell with niche cell
2) soluble factor: move, Hedgehog (maybe), Wnt
3) intermediate cell: stromal cells receive and send signal

134
Q

growth and differentiation of HSC

A

HSC divides and 1 cell leaves niche to become progenitor cell so asymmetric division

control fate by moving things around inside like proteins and growth factors - drive growth then differentiation

growth factors and cytokines act in paracrine fashion within tissue so diffuse and juxtacrine

so when move to diff niche get diff signal and send out diff signal

135
Q

specificity of differentiation of HSC examples

A

GM-CSF from lymphocytes (monocytes, macrophageS)

EPO from kidney, in RBC development

IL-3 to make basophils

136
Q

development of erythrocytes and platelets

A

early stage pass pathway generating MEP (megakaryocyte/erythrocyte precursor) then split

137
Q

erythropoiesis

A

generation of RBCs with EPO (erythropoietin) signal

MEP to proerythroblast to erythroblast (dividing) to reticulocyte (with nucleus, non-dividing) to RBC (non-dividing)

138
Q

thrombopoiesis

A

generation of platelets

TPO (thrombopoietin) initiates for megakaryocytes produced by liver

IL-6 doubles production by liver (stimulates thrombopoiesis)

in thrombocytopenia - decreased platelets, BM stromal cells produce TPO

platelets have TPO receptors so remove from circulation (-ve feedback)

139
Q

blood groups genotypes, phenotypes, alleles?

A

3 alternative alleles for 1 gene
6 genotypes
but 4 phenotype: A, B, AB, O

140
Q

why is it an AB group and not one or the other?

A

A and B are co-dominant

141
Q

ABO alleles

A

A/B dominant and O recessive so..

I^A
I^B
i^O

142
Q

what does I stand for in blood group alleles?

A

isoagglutinogen

143
Q

what do the enzymes encoded by blood group alleles do?

A

‘decorate’ carbohydrates on lipids (glycolipids) on RBCs (H-antigen attached to sphingosine to form glycolipid in group O, then more attached to this to form A and B)

O with Gal and Fuc
A with Gal, Fuc and Gal-NAc
B with Gal, Gal and Fuc

144
Q

glycosphingolipids

A

glycolipids with sphingosine

types:
cerebroside (ceramide with sugar residue) - stick in membrane, sphingosine group in membrane,
ganglioside (ceramide with chain of sugar residues)

145
Q

why does agglutination between blood groups occur?

A

diff blood groups express diff enzymes on surface of RBC
so A agglutinate B, AB no agglutinin Abs and O has both A/B Abs

so can mix AB with all blood types

146
Q

paternity of blood groups

A

same group as parents
but sometimes AB allele but phenotype O from epistasis - mutation means H-antigen can’t be made and H encodes FUT1 (Fucase transferase)

147
Q

secretor phenotype

non-secretors

A

77% Caucasians
water soluble A/B AGs in secretions (Se/Se or Se/se),
independent of blood type, encoded by FUT2

non: se/se with increased risk of oral disease, asthma, snoring, diabetes, alcoholism, infections, autoimmune

148
Q

MN blood groups

A

separate from ABO and don’t matter much because no natural Abs, so not affect transfusion

L^M and L^N are co-dominant

attachment site for plasmodium sp so malaria, encodes protein on RBC membrane

149
Q

Rh blood groups (Rhesus)

A

85% white Caucasians are Rh+
15% Rh-

many alleles, no natural Abs

3 genes on chromosome 1, 1 on chromosome 6

genotypes CDE, only cde/cde is rr and Rh- so triple mutant so rare

150
Q

haplotype

A

if carry 1 mutation, carry another because on same chromosome so inherit together, tightly linked so recombination can’t separate

151
Q

Rh incompatibility in pregnancy

A

Rh- female with Rh+ male first child is Rh+ so fine

but immunised in pregnancy so produce anti-Rh IgG so 2nd/3rd pregnancy causes haemolytic disease of foetus so still birth/neonatal death

can treat with anti-Rh Ab to prevent immunisation, or child blood transfusions

152
Q

ABO compatibility

A

anti-A/B IgM important in early pregnancy

female O male A (B,AB) more miscarriage than female A (B,AB) male O

153
Q

transfusions improvements

A 
storage
split products from RBCs
testing
anticoagulants
preservatives
refrigerate
blood bands
venous access
safety - contamination, allergic
154
Q

types of vessel formation

A

vasculogenesis
angiogenesis
lymphangiogenesis
arteriogenesis

155
Q

what usually causes angiogenesis

A

pathological process like trauma, embolism, neoplasia, diabetes, or regeneration of endometrium after menstruation, or just growth

156
Q

what are the 2 ways in which endothelial cells (ECs) grow in angiogenesis?

A

sprout

intussusceptive

157
Q

sprouting (angiogenesis)

A

something makes endothelium grow out
form lumen
another tube
pseudopodial processes guide sprout by migrating endothelial cells

158
Q

intussusceptive (angiogenesis)

A

endothelial cells grow down middle of tube to form 2 tubes,
requires cells to move away from ECM,
MMP enzymes break connections to form 2 capillaires with lumen in middle

159
Q

what is the process of triggering angiogenesis?

A

hypoxia - VHLp not oxidised so prevent binding to HIF-alpha so alpha binds beta and conformational change releases NLS so find target in nucleus

switch VEGF on - bind receptor on endothelial cells and drive proliferation and mitosis of cells,
express receptor for growth hormone so new capillaires
(and EPO synthesis for RBC formation)

160
Q

HIF-alpha/-beta

A

hypoxia-induced factor

destroyed in O2

161
Q

VEGF

A

vascular endothelial growth factor

a pro-angiogenic factor

162
Q

what happens in high O2 (angiogenesis)

A

no VEGF so VHL protein phosphorylated and hydroxylated to VHL-p-OH and binds to HIF-alpha so target to proteasome for destruction

163
Q

arteriogenesis

A

formation of arteries after blood flow obstruction (e.g. embolism clot or stenosis narrowing)

develop from pre-existing anastomosing (collateral) arterioles - anastomosis are small channels joining 2 large channels

164
Q

process of arteriogenesis

A

blood flow transfers from main arteries to anastomosing arterioles which response by enlarging (not just force more blood but growth driven by force and flow, NOT driven by O2)

shear stress and stretch detected by plasma membrane and cytoskeleton regulates cell shape change

SSRE (shear stress response element) indirectly activates genes like growth factors, adhesion molecules, proliferation of ECs so arterioles larger

165
Q

cytopenia and anaemia

A

cytopenia lack of cells so changed blood cell count

anaemia is fewer RBCs/ lack Hb in them

166
Q

types of anaemia

A

aplastic - few cells
iron deficiency - lack Hb
pernicious - vitamin B12 deficiency

167
Q

causes of anaemia

A 
bleeding
Hb synthesis defect
destroy RBCs by spleen
haematopoiesis defect
myelodysplasia - defect in lineage production
leukaemia
168
Q

symptoms of anaemia

A

enlarged spleen, yellow eyes (icterus)

169
Q

blood tests for anaemia

A

RBC/Hb low,
size smaller - MCV (mean corpuscular volume - RBC size), microcytic smaller when iron deficiency, macrocytic bigger when B12 deficiency

170
Q

how to treat anaemia

A

blood transfusions

cell transplant

171
Q

pacytopenia
leukopenia
neutropenia
thrombocytopenia

A

all cells reduced

WBCs reduced

neutrophils reduced

platelets reduced so not clot

172
Q

neutropenia

A

susceptible to infection

take FBC (full blood cell count) with differential (diff types of each cell counted)

can occur from chemo

173
Q

haematological neoplasia (+ 3 types)

A

new growth in blood

leukaemia, lymphoma, myeloma - depends on what overgrowth

174
Q

leukaemia

A

abnormal cells in BM so normal cell production pushed out, abnormal cells spill to circulation where don’t divide

175
Q

lymphoma

A

abnormal cells in lymph node and proliferate and spread to other nodes and destroy function, to other tissues and bone marrow, in secondary lymphoid tissues so from mature cells

e.g. B-cell neoplasms, T-cell and NK-cell neoplasms, Hodgkin lymphoma

176
Q

Hodgkin’s lymphoma

A

germinal B cells are owl like - swellings of overgrowth cause Reed Sternberg cells

blood counts are normal

enlarged nodes

high grade so need immediate chemo, quite treatable if early enough

177
Q

hypertension

A

high BP

persistent
>140/90

high even at rest

178
Q

where is arterial blood pressure measured in?

A

branchial artery

179
Q

white coat hypertension

A

anxious with doctor so increase BP

180
Q

overcoming white coat hypertension

A

at home measurements - ABPM (ambulatory blood pressure monitoring)

inflate every 1/2 hour and measure BP in clinic,
have all day during normal activity and when sleep, so 14 measurements

in clinic 2 per hour during waking hours and 14 total

at home: 3 measurements 1 min apart so take average, twice daily for 4-7 days and check both arms

181
Q

ausculation and korotkoff sounds and how to measure BP

A

body sounds when measuring blood pressure

1) inflate cuff and measure pressure in cuff, turn valve to turn pressure off so deflates,
pressure in cuff is line under red sound waves

2) pump cuff high to stop blood flow and hear no sound in arm
3) turn pressure off so blood flow again and 1st sound you hear is systolic pressure - 1st measurement, becomes louder as pressure decreases, sound stops means diastolic pressure - when flow normal

182
Q

auscultatory gap

A

sound suddenly stops during BP measurement

rare

if not pump cuff enough

183
Q

mean arterial pressure

A

60% diastolic and 40% systolic

(systolic + 2xdiastolic) divided by 3

184
Q

primary/essential hypertension (EH)

A

90-95% of all hypertension

probs complex genetics

185
Q

secondary hypertension

A

result of complications

186
Q

symptoms of hypertension

A

mostly none

headaches, dizzy, flushing, aware of heart beat, epistaxis (nose bleeds)

187
Q

clinical signs of hypertension

A

BP,
cardiomegaly/left ventricle hypertrophy (enlarges from high BP),
abnormal renal function

188
Q

hypertension complications

A 
risk of stroke
aortic aneurysm - swelling
heart failure
renal failure
end organ damage
189
Q

hypertension management

A

1) education/lifestyle changes
2) mostly drug treatment
3) surgery if 2ndary causes, underlying primary cause

190
Q

filling pressure

A

how much blood comes back to heart

191
Q

contractility

A

determined by adrenaline and noradrenaline on beta receptors

more blood the pump pushes out, the bigger the pressure and more muscle fibres stretched so pumps more

determines stroke volume

192
Q

stroke volume

A

how much blood per stroke

193
Q

cardiac output

A

determined by stroke volume + heart rate

194
Q

total peripheral resistance R

A

affected by diameter of arterioles

195
Q

blood pressure

A

cardiac output x total peripheral resistance

196
Q

controlling blood pressure (2, short term vs long)

A

short term: baroreceptor/sympathetic NS

long term: ECF volume/plasma renin activity

197
Q

baroreceptor reflex (if fall in blood pressure)

A

fall in blood pressure in detected by baroreceptors (pressure receptors) in carotid sinus which cause a decrease in nerve impulses to vasomotor centre in medulla so stimulate sympathetic and inhibit parasympathetic so increase heart rate and contractility and vasomotor tone and decrease diameter of blood vessels so increase resistance and increase venous return so more blood to venous system so increase BP

198
Q

treatment for hypertension: 2 ways to reduce it

A

reduce CO (stroke volume x heart rate): diuretics decrease BP, ACE inhibitors, Angiotensin II R antagonists, B-blockers

reduce TPR (total peripheral resistance): vasodilators to increase diameter, Ca channel antagonists, ACE inhibitors, Angiotensin II receptor antagonists, alpha-adrenoreceptor blockers

199
Q

what happens if hypertension drugs don’t work?

A

add another in combination instead of increasing dose

200
Q

ACE inhibitors

A

inhibit angiotensin converting enzyme so decrease arterial resistance and decrease blood volume and BP

side effects - rapid BP fall, persistent dry cough, no symptoms of hypertension so just makes you feel worse

201
Q

angiotensin II receptor antagonist (ARBs)

A

reduce BP by stopping affects of angiotensin II

well tolerated side effects, 1 daily dose, no dry cough, cost effective,

202
Q

calcium channel antagonists

A

block channels so vessels dilate and decrease TPR

cause headaches, flushing, ankle swelling

203
Q

thiazide diuretics

A

weak/mild and low dose

works on DCT to increase water and sodium LOSS so decrease blood volume and decrease cardiac output and mean arterial pressure

use in morning to avoid needed the toilet

can cause hypokalaemia - potassium supplements needed

most effective in elderly/African origin

204
Q

beta adrenoreceptor blockers (beta blockers)

A

no longer 1st line therapy

reduce contractility and decrease renin from kidney so decrease BP

non-specific so if block all beta receptors including bronchioles can induce asthma

can cause peripheral vasoconstriction so cold hands/feet

not effective in decreasing mortality, not sure why if reduces cardiac output

205
Q

study of angiotensin II receptor antagonist vs beta blocker

A

Lorsatan vs Atenolol (b blocker)
double blind
Lorsatan similar decrease in BP but better mortality and better tolerates

206
Q

alpha receptor blockers

A

vasodilation, fall in arterial pressure,
only used if resistant to other treatment

can cause postural hypotension

older drugs can cause reflex tachycardia because non-specific so block alpha2 as well

207
Q

malignant hypertension

A

accelerated and very high BP so emergency and need hospital

IV vasodilation, oral beta blockers, calcium antagonists

don’t use ACE inhibitors because rapid decrease in BP could cause cerebral infarction and blindness so need slow decrease

208
Q

myocardial infarction

A

heart attack

lack of blood flow to the heart

209
Q

angina

A

chest pain from lack of blood flow to the heart

210
Q

where is all the nutrients in the blood?

A

coronary arteries

little comes from the blood in chambers

211
Q

coronary circulation pathway (coronary venous drainage)

A

aorta to coronary arteries to smaller arterioles to veins to coronary sinus and back to right atrium

212
Q

phasic blood flow

A

heart contracts and blood flow reduces so relates the 2 and they are in phase

213
Q

how is coronary blood flow reduced?

A

decreased diastolic interval - more time in systole and flow reduced when contract

increased ventricular end-diastolic pressure - so pump blood against pressure gradient so reduce flow - if problems with heart congesting

fall in arterial pressure

214
Q

ventricular end-diastolic pressure

A

pressure at end of diastole measured in ventricle after filled with blood from left atrium

215
Q

how is coronary blood flow controlled

A

high O2 extraction occurs (70% of blood O2 removed as flows in heart) so can’t increase this to when need more O2, but increase blood flow instead

216
Q

coronary artery dilation

A

when more oxygen required

released vasodilator substances from cardiac muscle like adenosine potent dilator from ATP and K/bradykinin/H/CO2

217
Q

causes of atherosclerosis

A

genetic predisposition
excessive cholesterol in arteries
invade by fibrous tissue
plaques

218
Q

coronary syndromes

A

can predict because pain during exercise from not enough O2

stable angina, unstable angina, myocardial infarction

219
Q

stable angina

A

reduced blood flow but not block

220
Q

unstable angina

A

partially occlusive thrombus
occasionally bind and pain
unpredictable

221
Q

myocardial infarction

A

occlusive thrombus

ruptures so complete block

222
Q

what is the most common cause of morbidity and mortality?

A

heart attack (myocardial infarction)

223
Q

ischemia

A

loss blood supply so necrosis

224
Q

complete occlusion

A

dysfunctional endothelium so atherosclerosis and plaque rupture so occlusion

plaque causes turbulent flow so not straight through centre so build up on platelets when activated - causing thrombus occlusion

225
Q

infarction

A

blood flow ceases so only cholateral - blood flows around not in blood vessel so overfills with stagnant (still) blood and use up O2 so deoxygenated Hb,

vessel walls now highly permeable so fluid leaks and muscle cells swell and cardiac muscle cells die

226
Q

myocardial cell death

A 
from ischemia (no O2) so less ATP and less metabolism and impaired Na K ATPase,
increased H so increased Ca and increased membrane potential depolarisation so arrhythmias (messed up firing)
227
Q

collateral circulation

A

long time blockage causes vessels to bypass plaque and join around block but slow vessels but increases heart attack survival, takes years to develop

228
Q

causes of heart death

A

decreased cardiac output so cardiac shock

pulmonary oedema (fluid in lungs)

ventricular fibrillation (random beats)

heart rupture from thin/stretched walls

229
Q

cardiac shock (+systolic stretch)

A

insufficient force to pump blood so not enough supply round body

systolic stretch - bulging instead of pushing blood out so can rupture

death of peripheral tissues

decreased cardiac perfusion

230
Q

pulmonary oedema (excess fluid in lungs)

A 
reduced systemic blood circulation
pools in atria and vessels of lungs
increased capillary pressure in lungs
fluid in lungs
so less urine and increased total blood volume
231
Q

ventricular fibrillation

A

rapid disorganised electrical activity
dangerous in first 10 mins and 1 hr later

from K depletion, loss ATP, depolarise cells so fire, injury current (fire when die)

decreased BP causes sympathetic NS to activate and makes it worse

232
Q

diagnosis of heart problems

A

history - chest pain down to left arm

unrelated to excercise
ECG and biochemical markers

ischemia can cause severe pain

233
Q

ECG changes in heart

A

normally flat between QRS and T but now ST elevated

develop abnormal Q wave which may stay for life - injury current

234
Q

diagnosing full occlusive thrombus

A

heart attack and prolonged ischaemia

detect biomarkers in serum and ST elevation (STEMI)

235
Q

diagnosing transient ischaemia

A

no ST elevation, sometimes still biomarkers

236
Q

diagnosing partially occlusive thrombus

A

no ST elevation

sometimes serum biomarkers

237
Q

biochemical markers of myocardial infarction

A

troponins regulate muscle contraction
2 isoforms T and I

T structural skeletal muscle in utero

I catalytic only ever in myocardium

238
Q

treatment of heart attack

A

confirm diagnosis
relieve ischemic pain
stabilise haemodynamic abnormalities
save myocardial tissue

give O2 if hypoxic, restore flow by breaking thrombus

239
Q

recovery from myocardial infarction

A

dead fibres enlarge
non-function muscle recovers
dead absorbed by macrophages
fibrous tissue develops
gradual progressive contraction of fibrous tissue over the years,
hypertrophy of normal areas to compensate

240
Q

cardiac function after recovery

A

may be fine resting but bad when demand, decreased pumping capacity

normally 300-400% more blood per min than at rest, while now reduced to 100%

241
Q

angina pectoris (stable angina)

A

insufficient blood to heart, pain beneath upper sternum over heart

relieved with vasodilator and GTN

242
Q

treatment of stable angina

A

balance supply and demand but most work by decreasing demand

vasodilators reduce preload (blood coming back to heart) and decreased filling pressure so decreased demand for O2 and increase blood flow

surgery - aortic-coronary bypass surgery, coronary angioplasty to open vessel

243
Q

angioplasty

A

open vessel with balloon but plaque again so stent keeps plaque from reforming and drugs stop cells overgrowing around stent

Blood and Circulation (1 decks)

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