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Physio Lec > Cont 3 > Flashcards

Cont 3 Flashcards

(110 cards)

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1
Q

Increase RBC

A

Polycythemia

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2
Q

Decrease RBC

A

anemia

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3
Q

Cause anemia

A

Decrease erythropoiesis (NO Fe, NO vitB12, aplastic anemia/ bone marrow disease)

Increase erythrolysis (Hemolysis, hepatosplenomegaly)

Bleeding (acute-injury, chronic GI bleeding, menstruation, preg/delivery)

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4
Q

Def polycythemia

A

increase hematocrit with normal blood volum

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5
Q

Cause polycythemia

A

Primary: uncontrolled erythropoisis in bone marrow (Polycythemia Rubra Vera)/ cancer

Secondary: pathologically increase erythropoitein production - kidney (hypoxia b/c decrease local perfusion)

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6
Q

Polycythemia impact on circulation

A

increase hematocrit
increase TPR

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7
Q

Therapy polycythemia

A

traditional: remove/ dilut blood
current: eliminate stimuli/ suppression erythropoiesis

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8
Q

Type of anemia based on

A

chromic index

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9
Q

Hypochromic means

A

Fe dependent
Hypochromic microcyter anemia

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10
Q

Hyperchromic means

A

pernicious anemia

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11
Q

Normochromic menas

A

aplastic anemia

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12
Q

Hypochromic microcyte cause

A

NO/ malabs Fe
increase Fe requirement (pregnancy, lactation, rapid growth children)

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13
Q

Hypochromic microcyte symptoms

A

unspecific

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14
Q

Effect of hypochromic

A

decrease Hematocrit, HgB, MCV (cell size), MCH (amount HgB)
low ferritin, Fe in serum
increase total Fe binding capacity TIBC in blood - transferrin

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15
Q

Therapy hypochromic

A

oral Fe supplement
(food: total body Fe human: 3-4g
2/3 of it incorporated into heme erythrocytes)

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16
Q

Hyperchromic megaloblastic

A

NO B12 (rarely folic acid)
intrinsic factor deficiency:
Primary: NONE
Secondary: hypacidity, anacidity, alcoholism, tumor

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17
Q

Hyperchromic megaloblastic symptoms

A

Neurological: neuritis, dementia
Non specific: weight loss, pale, dry skin, diarrhea, soreness tongue, tendency for hemolysis

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18
Q

Effect Hyperchromic megaloblastic

A

decrease/ extremely low RBC no., hematocrit, HgB
increase MCV, MCH
peripheral smear: macrocytes

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19
Q

Therapy hyperchromic megaloblastic

A

parenteral
B12 supplement
folic acid
Fe
VitC

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20
Q

Normochromic, other types includes

A

hermorrhagic
hemolytic
aplastic
sicke cell anemia
thalassemia

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21
Q

Hermorrhagic

A

acute/ chronic blood loss

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22
Q

Hemolytic def

A

life span RBC decrease

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23
Q

Cause hemolytic

A

hemoglobin abnormal
bacterial. viral inf, autoimmune disease
toxins

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24
Q

aplastic

A

bone marrow disease -> reduced hemopoiesis

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25
Cause aplastic
tumor/ immune disease destruction bone marrow - infection, radiation, drugs/ toxins
26
Sickle cell anemia
mutation gene beta chain hemoglobin
27
Sickle cell anemia cause
mutation HgB link tgt -> stiff rods at low O2/pH -> form sickle cell increase malaria resistance
28
Thalassemia
reduce/ NO rate synthesis of 1 globin chains b/c mutation/ deletion reg region HgB genes high incidence in mediteranean region increase malaria resistance
29
Biliirubin
hydrophobic pigmented org anion
30
Billirubin solubility
water insoluble waste product
31
Cond for billirubin secretion
water soluble
32
Func billirubin meta
insoluble wate -> soluble -> excretes
33
formation billirubin
heme oxygenase (specific for alpha methylene bridge) -> billiverdin reductase (mammals only)-> billirubin
34
NO direct synthesis billirubin
35
Hemoglobin meta degrade
6g/day
36
hemoglobin meta form
300mg/day
37
Source formation billirubin
80% - breakdown senescent RBC 20% - others (myoglobin, catalase, peroxidase, cytochrome)
38
affinity billirubin, albumin
billirubin - low affinity albumin -> easily detach -> enter tissues
39
what displaces bilirubin
sulphonomides/ salicylates/ penicllin/ others acidosis
40
effect after displace billirubin from albumin binding sites
kernicterus (brain dys, permanent damage) mainly in newborns, adult: rare
41
Pathway billirubin trans in blood
blood - RBC + Hb -> spleen -> Hb to Bi -> blood -> Alb + Bi
42
Conjugation pathway billirubin
blood - Alb + Bi -> liver -> Bi +Glu (lipid soluble) -> BiDG (water soluble)
43
Conjugation billirubin activator
phenorbarbital (billi -> barbi -> activates)
44
Conjugation billirubin inhibitor
primaquine chloramphenicol androgen pregnanediol
45
solubility, binding, filtration, rxn unconj (indirect reacting billirubin)
unconj: lipid soluble bind to albumin NO filtrates thru glomeruli NO pos rxn in diazol probe
46
solubility, binding, filtration conj (direct reacting billirubin)
conj: water soluble NO bind albumin - conjugated to glucoronic acid filtrates thru glomeruli pos rxn in diazol probe
47
Detection bilirubin conjugated by van den bergh
yellow -> + diazol reagent -> orange (azobillirubin) -> colorimetric measurement -> direct billirubin (conj)
48
Detection total billirubin by van den bergh
yellow -> +alcohol (yellow) -> + diazol reagent -> orange (azobillirubin) -> colorimetric measurement -> total billirubin
49
formula indirect billirubin
total billirubin - direct billirubin -> indirect billirubin
50
Hemoglobin meta makes stool
BiDG -> bile duct -> small intestine -> Ubg (colourless) -> Stbg -> Stb (brown) -> stool
51
Hemoglobin meta makes urine
BiDG -> bile duct -> small intestin -> Ubg (colourless) -> blood -> kidney -> Ub (yellow) -> urine
52
Recycle Ubg
absorp in liver
53
Normal value serum total billirubin
1.71 - 20.5 umol/L
54
Normal conj billirubin
<5.1 umol/L
55
Hyperbillirubinemia cause
increase plasma conc (30-40umol/L) billirubin b/c imbalance production, excretion
56
Clinical name hyperbillirubin
jaundice (icterus)
57
Types jaundice based on abnormality
prehepatic/ hemolytic hepatic posthepatic/ obstructive
58
Cause prehepatic/ hemolytic
increase any value in blood of RBC, Hb,... -> increase everything else
59
Cause hepatic jaundice
abnormal abs liver -> BiDG into blood -> kidney (normal: BiDG NO into kidney)
60
Cause post hepatic jaundice/ obstructive
Obstruction bile duct -> BiDG into kidney
61
Serum bilirubin, urine billirubin, serume urobillinogen Ubg, urine Ubg, stool Prehepatic
increase (indirect) (same for all 3 cases) NO (only here) increase (same for first 2) increase (same for first 2) dark
62
Serum bilirubin, urine billirubin, serume urobillinogen Ubg, urine Ubg, stool hepatic (hepatitis)
increase (indirect, direct) YES - dark urine (same for hep, posthep) increase increase dark less significant
63
Serum bilirubin, urine billirubin, serume urobillinogen Ubg, urine Ubg, stool posthep
increase YES - dark urine decrease decrease gray
64
Classification jaudice based on type billirubin: unconj
in newborn Prehepatic: hemolytic ; non hemolytic
65
Classification jaudice based on type billirubin: unconj + conj
hepatic (hepatitis, viral, alcoholism)
66
Classification jaundice based on type billirubin: conj
posthepatic (obstruction, pancreas cancer) congenital: Dubin-Johnson syndrome: defect excretion Bi Rotor's syndrome: defect excretion Bi
67
Neonatal jaundice
in newborn common in premature infants
68
Cause neonatal jaundice
immaturity enzymes in billirubin conj (UDP glucuronyl transf) limited substrate UDB-glucoronuc acid -> unconj high in serum -> cross blood brain barrier -> Kernicterus (mental retardation)
69
Therapy neonatal jaundice
phototherapy blue light -> convert billirubin -> water soluble non toxic isomer (lumirubin) -> excrete thru urine
70
Bile concentration in gallbladder by movement H20, electrolytes
71
Bile secretion by liver:
0.8-1L/day
72
Volume gall bladder
15-60ml
73
Billirubin in liver bile
100mg/100mL
74
Billirubin in gallbladder bile
1000mg/100mL
75
Types gallstone
cholesterol type pigment type
76
Pigment type gallstones
brown, crumbly cause: excess billirubin consequences: bacterial/ parasitic infection in billary tree bacterial beta glucuronidase hydrolyze conj billirubin -> free form -> ppt -> calcium billirubinate
77
Urine in prehepatic, hepatic, posthepatic
pre: yellow hep: darker pre post: darker than pre darker b/c YES billirubin urine
78
billirubin structure
profirin deriv. (heme) NO Fe
79
Muscle types based on speed contraction
fast slow
80
Muscle types based on source energy
oxidative glycolytic
81
classification skeletal m.
1. slow oxidative 2B. fast glycolytic 2A: fast oxidative (OGO)
82
Myosin isoenzyme (ATPase rate), SR Ca2+ pumping capacity, Dia, OX capacity (mitch content, capillary density, myoglobin), Glycolyitc capacity, mech response 1.Slow OX
slow (slow OX -> myosin rate slow) moderate (slow -> dont need to pump much) moderate (1.2.3.: moderate - large - small) high (name is OX -> high) moderate (name is slow OX -> glycolytic moderate) slow (slow -> slow)
83
Myosin isoenzyme (ATPase rate), SR Ca2+ pumping capacity, Dia, OX capacity (mitch content, capillary density, myoglobin), Glycolyitc capacity, mech response 2. Fast Glycolytic
fast (name is fast -> fast) high (fast -> need high pumping) large (dia 1.2.3. moderate - large - small) low (name is glycolytic -> OX low) high (name is glycolytic -> glycolytic capacity high) fast (name is fast -> fast) (glycolytic: need fast NOT E)
84
Myosin isoenzyme (ATPase rate), SR Ca2+ pumping capacity, Dia, OX capacity (mitch content, capillary density, myoglobin), Glycolyitc capacity, mech response 3. fast OX
fast (name is fast -> myosin fast) high (name is fast -> pumping high) small (dia 1.2.3. moderate -> large -> small) VERY high (name is OX -> OX capacity high ; FAST Ox -> very high) high (Exception, if sees Fast -> glycolytic capacity is high GF - glycolytic -fast) fast (name is fast -> fast response)
85
Effect of physical exercise
increase rate meta
86
pathway skeletal muscle in physical exercise
review pics
87
Effect increase O2 consumption
resp rate increase tidal volume increase O2 diffusion alveoli increase max stoke volume increase max AV O2 diff increase
88
Local reponses to physcical exercise
increase blood perfusion working muscle VD (b/c symp cholinergic activty) VD (b/c increase meta - hypoxia, hypercapnia, acidosis) increase AV O2 diff (O2 extraction)
89
Changes in systemic circulation physical exercise
increase HR increase SV (> pronounced in the beginning) -> increase CO -> increase pA decrease peripheral resistance (b/c VD) redistribution circulating blood volume increase flow pulmon. vessels reg hypercapnia, hypoxia, acidosis -> reflexes
90
Cardiovascular para associated with exercise
increase EDV (b/c VR increase) decrease ESV (b/c CO increase -> blood in sys decrease) decrease dia pressure (b/c VD -> decrease TPR) increase sys pressure MAP increase
91
Distribution blood among organs with exercise
muslce blood flow increase splanchnic blood flow decrease brain, heart blood flow stays the same skin blood flow increase - symp cholinergic VD skin blood flow decrease - symp adrenergic a1 VC
92
Adaptation resp system to exercise
increase resp freq increase resp volume increase rep minute volume (resp freq * resp volume)
93
Value increase resp freq
15/min -> 40-50/min
94
Value increase resp volume
0.5L -> 3L
95
Value increase resp minute volume
7-8L/min -> 150L/min
96
Regulation resp system during exercise thru
reflexes (+) by hypercapnia, hypoxia
97
Adaptation resp to intermediate intensity exercise
MAP pO2 NO change significantly MAP pCO2 NO change significantly venouse O2 conc decrease (b/c increase usage O2)
98
Oxygen debt aka
exercise -> increase O2 use
99
Why need to increase O2 use after exercise
replenish O2 stores replenish phosphocreatine pool (cut phospho and creatin - direct phos) eliminate lactic acid (eli needs O2)
100
fast glycolytic another name
fast twitch m.
101
charac fast glycolytic m.
white appearance
102
Components m. energetics
Phosphagen systsem (8-10s) Glycogen-lactic acid system (1-2min) Aerobic system (unlimited time - as long as nutrients last)
103
Speed contraction depends on
load
104
speed muslce formula
105
speed depends on load . Contraction:
isotonic contraction isometric contraction
106
Performance formula
P= F*v
107
Performance m. depends on
load
108
Charac of performance
bell shaped curve -> optimal load efficiency - 20%
109
Performance/ power skeletal muscle reaches max
reaches max at 1/3 max attainable force
110
NO surfactant effect on pH
arterial blood pH acidic

Physio Lec (5 decks)

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