Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Physio Lec > Physio cont 4 > Flashcards

Physio cont 4 Flashcards

1
Q

shock effect

A

inadequate organ perfusion, tissue O2nation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Func org perfusion

A

deliver O2, nutrients
remove metabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

shifts when hypoxia

A

shifts to anaerobic pathway -> cellular dys, organ failure, damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Tissue hypoperfusion

A

relates to cardiovascular, neuroendocrine responses -> compensate, revers inadequate tissue perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Factors influecne tissue perfusion

A

Q=P/R
Flow= pressure gradient/ resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Microcirculation depends on

A

constriction precap, postcap vessles
intense hypoxia -> VD arterioles
VC -> intravas fluid loss
increase cap permeability -> tissue edema
adhesion leuk + platelets on epi lesions
intravas coag.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Types of shock

A

hypovolemic
cardiogenic
obstructive
distributive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Def hypovolemic shock

A

intravas fluid volume loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

cause hypovolemic shock

A

hemorrhage (xuat huyet)
dehydration by: vomitting, diarrhea, extreme sweating, burns
trauma: concussion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cardiogenic shock def

A

dys heart pump
(cardio - heart)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

cause cardiogenic shock

A

decrease pump func by: ischemia, anoxia, cardiomyopathy

valve disease: obstructive, regurgitant flow

dysrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Obstructive shock def

A

factors extrinsic to cardiac valves, myocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cause obstructive shock

A

venous return decrease: pericardial tamponade, v.cava obstruction, pneumothorax, pulmon embolism, coarctation aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Def distributive shock

A

pathological redis intravas fluid volume
excessive dilation blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

subtypes distributive shock

A

neurogenic shock
anaphylactic shock
septic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

cause neurogenic shock

A

spinal transsection
brain damage
fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

cause anaphylactic shock

A

VD
increase cap permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

cause septick shock

A

endotoxins
VD, fever, DIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

stages of shock

A
  1. non progressive - compensated
  2. progressive - decompensated
  3. irreversible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Stages of shock ATP

A
  1. ATP supply = ATP demand
  2. ATP supply < ATP demand
  3. ATP supply &laquo_space;ATP demand

review pic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Cellular effects of inadequate tissue perfusion - anaerobic meta

A
  1. glycolysis -> ATP depletion
    -> NA+/K_ ATPase slows
  • [Na]IC acc.
  • cell swelling -> decrease EC volume
  • mitch, ER swelling
  • changes membrane potential [Ca2+]IC
  1. acc. lactic acid -> pH IC decrease
  2. acc. inorg P -> pH IC decrease
  3. acc. O2 radicals
  4. synthesis enzymes, structural proteins decrease
  5. apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Def stage 1 non progressive/ compensated

A

normal circulatory compensatory mech -> full recovery w/o outside therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Degree of symptoms stage 1 non progressive/ compensated

A

depends on smount blood loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Symptoms non preogressive/ compensated

A

pale, cold, sweaty skin
rapid breathing
tachycardia, weak pulse
blood pressure MAINTAIN (Psys maintain, Pdia increase)
mildly anxious, restless, irritable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Key response of body of stage 1 non progressive/compensated
neg feedback - compensation return CO, MAP to normal level
26
Activation neg feedback (neuroendocrine) based on
time: sec ; min/hr
27
activation neg feedback sec
Baroreceptor reflex Chemoreceptor reflex CNS ischaemic response
28
activation neg feedback min/hr
Cardiopulmonary baroreceptor reflex RAS ADH/Vasopressin ANF
29
Baroreceptor
decrease MAP -> high pressure baro (carotid sinus, aortic arch) -> CN9,10 -> CVLM -> (-) RVLM -> (+) SNS fibers -> (-) CN10 -> heart, arteriole, adrenal medulla -> Pressor response
30
Chemoreceptor reflex - from PCR
decrease pO2 (MAP<80mmHg) -> PCR (carotid, aortic bodies = low baro) -> RVLM(resp center) -> hyperventillation -> RVLM -> SNS fibers -> heart, arterioles, v. adrenal medulla -> pressure (chemo -> scared -> breathe more -> hyperventillation)
31
orthostatic position
at level skull MAP 10-15mmHg < heart
32
CNS ischaemic response
decrease MAP (<60mmHg - lower than chemo) cerebral blood flow decrease -> ischemia -> direct action -> RVLM -> SNS fibers -> sys arteries (NOT to coronaries, brain) -> increase increase increase MAP -> maintain flow (ischaemic - lost blood -> no time to waste -> direct action to RVLM -> sys arteries except coronarie, brain -> increase MAP a bunch)
33
Cardiopulmon. baroreceptor reflex
decrease blood volume decrease VR -> cardiopulmon baro -> viscerosensory n. -> NTS -> decrease CVLM -> increase RVLM -> SNS increase -> angiotension2 increase ; VC ; increase MAP -> hypothalamus -> increase ADH (cardio -> relates to heart -> decrease blood volume, VR)
34
Long term reg factors AT, ADH
decrease plasma volume decrease MAP -> increase Renin, increase AT2 -> increase ADH/VP -> decrease ANF increase plasma volume increase MAP
35
Role of SNS
neg feedback
36
effect increas SNS to heart
increase SV increase HR increase CO
37
effect increase SNS to coronaries
indirect way VD (SNS dont want to hurt coronaries -> VD) increase flow
38
effect increase SNS to kidney, GI, skin
VC increase TPR decrease flow
39
Effect increase SNS
maintain MAP
40
effect increase SNS to veins
VC increase VR increase Starling increase SV increase CO
41
Neuroendocrine responses during circulatory shock
CRH (Corticotropin releasing hormone) increase ACTH release (adenocorticotropin hormone) Cortisol release - adrenal cortex Adrenalin, Noradrenalin - adrenal medulla Glucagon increase, insulin decrease - pancrease ADH/ vasopression - pituitary gland catabolic hormones -> energy source for cells -> vasoactive substances -> increase MAP
42
Def progressive - decompensated
circulating system deterioate w/o therapy -> worsen till death
43
Symptoms pregressive
pale, cold, sweaty skin marked tachycardia, weak pulse low blood pressure (Ps < 100mmHg) increase shock index (HR/Psys >0.5) empty neck v. altered mental status (confusion, anxiety, agitation) thirst oliguria
44
feedback of progressive- decompensated
pos feedback -> circle of progressively decrease CO, MAP
45
blood supply of progressive- decompensated
to most imp organs only
46
Effect of progressive/ decompensated
Tissue damage: heart: decrease CO kidney: uremia CNS: vasomotor failure lysosomes, acidosis, decrease ATP Blood: increase thrombosis (DIC) (blood clotting) endothelial collapse
47
Charac progressive/ decompensated
need therapy
48
stage 3 irreversible def
all forms known therapy NO save still alive in this moment
49
irreversible shock stage symptoms
cold, sweaty, extremely pal (moribund) skin extreme tachycardia (>140) NO/rare palpable pulse blood pressure decrease confusion, unconsciouness anuria
50
Effect therapy to stage 3 irreversible
despite therapy - still deteriote: therapy resistant cardiac depression (falling Psys, Pdia) cap dilation, increase permeability
51
Tissue damage stage 3 irreversible
excessive, irreversible
52
effect of tissue damage stage 3 irreversible
endothel dys macrophage -> inflammation microcirculation failure advanced disseminated intravas coagulation
53
Therapy of shock
head down postion(Tredelenburg) Haemorrhagic arrest replacement therapy: saline, dextrane O2 therapy Corticosteroid: increas SV, stabilize lysosome membrane antihistamine pain relief sympathomimetic drugs
54
Coagulation clotting factor
Calcium 11 diff proteins (coagulation factors): proenzymes (inactive enzyme) -> active enyme need for clotting synthesis need Vit K
55
Location formation clotting factors
liver
56
How coag factors active
in proteolytic cascade
57
Types proteolytic cascade
Intrinsic: (+) in blood stream - contact activation Extrinsic: (+) from outside vascular bed - trauma Common pathway: formation fibrin network
58
Fribrinolysis starts when
right after coag completed (-> reparation damaged vascular bed)
59
Relation ship 3 cascade
Intrinsic pathway -> common pathway Extrinsic pathway -> common pathway
60
Extrinsic/ Tissue factor pathway activation, location
(+) by tissue factor outside vascular bed, trauma
61
What are tissue factors, expressed by
membrane receptor expressed by sub-endothelial cells ( smooth m., fibroblasts) upon injury
62
Ex tissue factor
Thromboplastin CD142
63
Pathway mech extrinsic
damage vascular endothelium -> blood contact extravas tissue -> (greater damage -> more tissue factor released) -> TF + Ca2+ Factor 7 -> facilitate 7 -> 7A [7a + 10 -> 10a] -> (+) 7A
64
Tissue factor of diseminated intravas coagulopathy DIC
membrane receptor expressed by sub-endothelial cells (smooth m., fibroblast upon injury) expressed by endothelial cell upon bac infection, inflammation
65
initiation intrinsic/ contact activation pathway
(+) proenzymes (Factor7) exposed to non hydrophobic surface (collagen, activated, any strange surface like glass)
66
Pathway formation intrinsic pathway
7 -> 7a (contact activation) -> 1st complex prekallikrein -> Kallikrein -> 1st complex HMWK (high molecular weight kinninogen) -> 1st complex ->1st complex + 11 -> 11a -> 11a+9 -> 9a -> Tenase complex 8 +7+7a+5a+thrombin -> 8a -> tenase complex PL -> tenase complex Ca2+ -> tenase complex (ten -> 10a - ase) tenase complex + 10 -> 10a
67
Func common pathway
forms fibrin network
68
Formation fibrin pathway
Intrin, extrinsic pathway -> prothrombinase complex (10a,5a,PL,Ca2+) -> (+) Prothrombin to Thrombin -> converts soluble fibrinogen -> insoluble fibrin -> 3d network crosslinked -> trap cellular elements
69
Interxn btw intrinsic, extrinsic pathway
damage blood vessels -> (+) extrinsic (thromboplastin), (+) intrinsic (non hydrophobic surface)
70
Charac activation extrinsic pathway
faster (substrate from extravas space): small clot formed quickly
71
Charac activation intrinsic pathway
longer cascade - high amp: slower, > powerful
72
Extrinsic, intrinsic pathway - additive charac
73
What happens after formation clot
Clot retraction Fibrinolysis
74
Clot retraction mech
fibrin meshwork formed -> RBC, platelets stick to firbin trands -> platelets contract -> clot retraction
75
Clot retraction def
pulls torn edges vessel closer tgt -> reduce residual bleeding -> stabilize injury site reduce size injured area -> easier for fibrblast, smooth m. cell, endothelial cells -> complete repair
76
Fibrinolysis def
repairs proceed -> clot gradually dissolves
77
Fibrinolysis mech enzyme
(+) proenzyme plasminogen by Thrombin: (+) in common pathway Tissue plasminogen activator: released by damaged tissue
78
what helps fibrinolysis
plasminogen -> plasmin -> digest firbin strands -> erodes foundation clot
79
-> Coagu <-Fibrinolysis
Fibrinogen + Thrombin -> Fribin poly + Plasmin -> Fibrin fragments (TP)
80
Func endothelium in hemostasis
intact endothel (-) activation agg platelets (adenosine, NO, PGI2) (-) thrombin activation -> reg normal balance btw hemostasis, fibrinolysis
81
Factors results in injury endothelial
post ischemic reperfusion acut, chronic infl atherosclerosis diabetes chronic hypertension
82
Manipulating hemostasis - in VITRO anticoag.
citrate, EDTA -> binding Ca2+ ions light blue - contain measured amount citrate purple/ lavender: contains EDTA
83
Manipulating hemostasis - in VIVO
imp anticoagulant drugs: Heparin, LMWH (intrinsic) -> (-) thrombin by (+) antithrombin Vit K antagonists Warfarin (Coumadin) Acenocoumarol Phenprocoumon Phenindione Aspirin -> (-) platelets agg. (higher amounts increase bleeding time)
84
Streptokinase
helps fibrinolysis b/c plasminogen -> plasmin (by thrombin + streptokinase)
85
Pathological con. hemostasis
Hemophilia (coagulation factors missing) Thrombophilia (risk of thrombosis) Plaque
86
Cause hemophilia (coag factor missing)
8 - hemophilia A - by X chromo - most common 9 - hemophilia B - by X chromo NO 7 5
87
Cause thrombophilia (risk of thrombsis)
antiphospholipid syndromes protein S,C defects Leiden mutation 5 -> gain func
88
Cause plaque
acc. lipids in subendothelial CT -> inflam -> thrombus -> detached fragments: emboli
89
Development RBC erythrocytes origin
Multipotential hematopoietic stem cell (Hemocytoblast HSC) Common nyeloid progenitor (CMP)
90
Charac of erythrocytes deve
proliferate self renewal
91
structure deve RBC
have macrophage reticular (mesh like) ribosomal RNA
92
what are degrades in RBC
membrane MHC1 nucleus
93
Factors determine rate erythropoiesis
erythrpoietin Fe Vit12 - folic acid Nutritional state body
94
Location production erythropoitetin
kidney
95
(+) erythropoiesis - Hb synthesis
ACTH Androgens Steroids (ErythropoieiS -> A -> ACTH, Androgens -> S -> steroids)
96
(-) erythropoiesis - Hb synthesis
estrogen reduced O2 demand
97
Hypoxia in kidney inhibits by
erythropoiesis - Hb synthesis reduced O2 demand (hypothyreosis) (tạo máu -> ko thiếu máu -> ko thiếu O2 kidney) (ko cần dùng O2 -> ko đc thiếu O2 kidney)
98
Hypoxia kidney activates
increase eythropoietin secretion (transcriptional reg mRNA) (thiếu O2 - thiếu máu -> tạo nhiều máu)
99
What activates hypoxia kidney
anemia hystotoxic effects reduced blood flow decrease O2 sat in blood Increase O2 demand (thyreotoxicosis) (thiếu máu, toxic shock, thiếu O2, cần nhiều O2(thyreotoxicosis) -> activates hypoxia kidney)
100
Pathway Fe in erythropoietic
1. Fe2+, Fe3+ ingested 2. Fe3+ + HCl -> Fe2+ 3. Fe2+ binds gastroferritin (GI) 4. Gastroferritin transport Fe -> small intestine 5. Fe absorbed from GI tract -> blood plasma 6. Fe binds transferrin (blood) 7. Fe binds apoferitin (liver) -> enterocytes -> stored as ferritin 8. Fe distributed to tissues (GTA game - Gastroferitin (GI) -> Transferrin (blood) -> Apoferritin (liver) -> stored as ferritin
101
Total body Fe in human adult
3-4g 2/3 into heme of erythrocytes
102
Fe2+ absorp in
dudodenum jejunum
103
Compartments, cycle Fe
4 compartments 1. heme containing O2 trans protein 2. Storage compartment 3. Trans compartment 4. Fe containing enzymes
104
compartment 1: heme containing O2 trans protein
haemoglobin 2/3 total body Fe, myoglobin
105
compartment 2: storage compartment
Ferritin, hemosiderin 1/4 total body Fe (Ferritin -> fourth -> 1/4) 1/2 storage compartment: Ferritin + half hemosiderin Ferritin > readily available
106
compartment 3: transport compartment
plasma contains small fraction body Fe stores plasma Fe bound to transferrin Non transferrin - toxic, in Fe overload when Fe binding capacity transf exceeded turnover times: 6-8/day
107
compartment 4: Fe containing enzyme
ex: cytochroms, catalase, peroxidase, ribonuclease reductase
108
Vit B12 cobalamine charac
water soluble corrinoid ring - similar to pofirin only some bacteria, protozoa synthesize (imp of colon bacteria) in meat, liver, egg, milk NO in plants nicotine reduce absp daily requirement: 1-2ug store in liver for 3-6 yrs.
109
Pathway mech VitB12 cobalamine
pics trans in, out blood stream goes thru enterocytes by receptor mediated endocytosis (recognizes dimer)

Physio Lec (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions