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AET 310 > FINAL EXAM > Flashcards

FINAL EXAM Flashcards

1
Q

where are platelets derived from?

A

megakaryocytes in bone marrow

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2
Q

how long do platelets last?

A

8-9 days in circulation

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3
Q

where is platelts stored and how much

A

1/3 stored in the spleen and released when needed

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4
Q

what stimulates platelet production

A

thrombopoietin

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5
Q

where are platelets made

A

liver, kidney, smooth muscle, bone marrow

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6
Q

do platelets have a nucleus?

A

no

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7
Q

what do a-granules contain?

A

fibronogen, coagulation factors, plasminogen, PAF and PDGFs

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8
Q

what do δ-granules contain?

A

ADP, ATP, Ca2+, serotonin and histamine

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9
Q

All but which of the following are true about platelets?

A. An enzyme called erythropoietin stimulates their
production. B. They are made from megakaryocytes. C. They originate from the bone marrow. D. They are stored in the spleen

A

A

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10
Q

what do plasma proteins circulate as

A

inactive procoagulation factors

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11
Q

where are plasma proteins synthesised

A

most are by the liver

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12
Q

when is ca2+ (factor IV) required?

A

in all but the first two clotting steps

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13
Q

steps of clot dissolution

A

Antithrombin III, proteins C & S, plasminogen –> plasmin
(digests fibrin strands)

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14
Q

The endothelial surface prevents?

A

platelets & plasma
coagulation factors from interacting with the underlying
thrombogenic subendothelial ECM

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15
Q

Healthy, intact endothelial cells normally produce several
substances that prevent platelet adhesion & aggregation

A
  • PGI2
    – NO
    – ADPase
    – tPA
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16
Q

stages of hemostasis

A

1) Vessel spasm
2) Formation of the platelet plug
3) Blood coagulation or development of an insoluble fibrin
clot
4) Clot retraction
5) Clot dissolution

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17
Q

stage 1 of hemostasis

A
  • MOI: Local and
    humoral
    mechanisms * Transient (<1 min)
  • Vascular smooth
    muscle contracts
    to decrease blood flow
  • Local neural
    reflexes & humoral
    factors (TXA2
    from
    platelets)
    contribute to
    vasoconstriction
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18
Q

stage 2 of hemostasis

A
  • vWF (from endothelium)
    causes adhesion of
    platelets to exposed
    collagen of vessel wall
  • Platelets become
    activated & release ADP
    & TXA
    2
    which causes
    platelet aggregation &
    formation of a plug
    (therefore aspirin acts as a platelet aggregation inhibitor)
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19
Q

stage 2 hemostasis

A
  • Insoluble fibrin threads hold the clot together
  • Anticoagulants such as heparin (mast cells) act to prevent
    excessive fibrin formation (ie. decrease clotting)
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20
Q

stage 4 hemostasis

A
  • Within 20-60 mins
  • Actin & myosin in
    platelets contract to
    squeeze serum from
    the clot & join the
    edges of the broken
    vessel
  • Failure of clot
    retraction indicative
    of a low platelet
    count
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21
Q

stage 5 hemostasis

A
  • “Fibrinolysis”: Allows
    blood flow to be re-
    established & tissue
    repair to take place;
    strands of the clot are
    dissolved
  • Plasminogen activators
    such as tPA & uPA
    cause formation of
    plasmin, which digests
    the fibrin strands of the
    clot
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22
Q

what is fibrinolysis

A
  • “Fibrinolysis”: Allows
    blood flow to be re-
    established & tissue
    repair to take place;
    strands of the clot are
    dissolved
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23
Q

hypercoagulability

A

Conditions that predispose to thrombosis & blood vessel
occlusion

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24
Q

two forms of hypercoagulability

A
  1. increase platelet function
  2. increase clotting acitivity
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25
Q

increase platelet function

A
  1. increase platelet function
    – increase platelet # (thrombocytosis)
    – Blood flow disturbances Caused by
    – Endothelial damage atherosclerosis
    – Platelet aggregation
    (last 3 are caused by atherosclerosis)
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26
Q

increase clotting activity

A

– increase procoagulation factors
– decrease anticoagulation factor

1.inherited or
2. aquired by prolonged bed rest, smoking, obesity etc

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27
Q

true or false
Hypercoagulability states increase the risk of thrombus
formation.

A

true

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28
Q

decrease in platelet levels (thrombocytopenia)

A
  • decrease production in bone marrow
  • increase destruction due to antiplatelet Ab’s
  • Platelets used up in forming excessive clots
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29
Q

decrease platelet FUNCTION (thrombocytopathia)

A
  • Inherited (vWF disease) or acquired (aspirin &
    NSAID use which decreases TXA2
    production)
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30
Q

Coagulation disorders (2)

A

– Inherited: eg. vWF disease (decrease vWF) or Hemophilia A
(decrease factor VIII)
– Acquired: liver disease or vit K deficiency

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31
Q

COX-1 catalyzes

A

production of thromboxane A2

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32
Q

COX-2 catalyzes

A

production of prostaglandins

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33
Q

what inhibits COX-1 and COX-2?

A

Aspirin and NSAIDs

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34
Q

why is aspirin used as a blood thinner

A

prevent blood cells called platelets from clumping together to form a clot

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35
Q

why is “blood thinner” not the best description

A

they don’t actually make blood thinner

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36
Q

What is the effect of von Willebrand disease on the
platelets?

A

decreased platelet adhesion

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37
Q

true or false

Platelet disorders are likely to lead to excessive bleeding

A

true

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38
Q

Spectrin/ankyrin network
imparts

A

both elasticity &
stability to the RBC

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39
Q

Adult (HbA) vs. fetal Hb
(HbF) forms

A

HbF has a higher affinity
for O2

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40
Q

RBCs rely upon what to make ATP

A

anaerobic
glycolysis to make ATP

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41
Q

How many molecules of oxygen can be carried by one
molecule of hemoglobin?

A

Four (each hemo has 2 alpha and 2 gamma molecules)

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42
Q

what does affects the rate at which Hb is made?

A

depends on Fe availability

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43
Q

how much Fe is found in Hb

A

~65%

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44
Q

how much Fe is stored in a different place and where?

A

~15-30% stored in liver and reticulo-endotherlial cells of bone marrow

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45
Q

transferrin

A

Fe transporter in plasma

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46
Q

Ferritin

A

a protein-Fe storage Complex (mainly liver)
- serum ferritin levels = index of body iron stores

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47
Q

RBC lifespan

A

~ 120 days

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48
Q

bilirubin

A

a yellowish pigment that is made during the breakdown of red blood cells

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49
Q

jaundice

A

if RBC destruction >
ability of liver to remove bilirubin
from blood

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50
Q

Haptoglobin

A

a protein made by your liver. and will bind the excess plasma Hb

If overwhelmed
(water soluble)
hemoglobinemia and/or
hemoglobinuria can result

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51
Q

hemoglobinemia

A

a medical condition in which there is an excess of hemoglobin in the blood plasma

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52
Q

hemoglobinuria

A

if the level of hemoglobin in the blood rises too high, then hemoglobin begins to appear in the urine.

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53
Q

Why would someone with renal failure develop
anemia

A

because there is a lack of EPO

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54
Q

MCV (mean corpuscular volume)

A

decrease with microcytic & increase with macrocytic anemias

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55
Q

MCHV (mean corpuscular hemoglobin concentration)

A

Normochromic & hypochromic anemias

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56
Q

microcytic and macrocytic

A

Microcytic cells are smaller than normal size, especially in the setting of iron-deficient anemia and anemia of chronic disease. Macrocytic anemia is a type of anemia where the average red blood cell volume is larger than normal

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57
Q

Normochromic & hypochromic

A

Erythrocytes containing the normal amount of hemoglobin (normal MCHC) are called normochromic. When the MCHC is abnormally low they are called hypochromic

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58
Q

Red blood cells (erythrocytes) are made in the ________
and destroyed in the _________.

A

bone marrow, spleen

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59
Q

Iron Deficiency anemia

A

Common worldwide cause of
anemia affecting persons of all ages
* Chronic blood loss or deficient diet
* decrease Hb and Hct
* decrease serum Fe and ferritin
* Hypochromic and microcytic
erythrocytes
* Poikilocytosis (irregular shape)
* Anisocytosis (irregular size)
* Depending on severity: pallor,
fatigue, dyspnea, tachycardia

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60
Q

Megaloblastic Anemia

A

caused by decreased DNA synthesis:
– Vitamin B12
and folic acid deficiencies
(both are needed for DNA synthesis) – Impaired DNA synthesis –> enlarged
red cells
– RBCs are large, often with oval shape

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61
Q

Aplastic Anemia

A

Aplastic due to disorder of pluripotent BM stem cells
– Usually leads to decreased RBCs, WBCs & platelets
– Causes: radiation, chemotherapy, chemicals, toxins,immunological problems, idiopathic.
– Tx: blood transfusions, bone marrow transplant

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62
Q

Which type of deficiency is caused by pernicious anemia?

A

vitamin B12

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63
Q

what is polycythemia

A

increase RBC count and Hct >50%

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64
Q

relative polycythemia

A

decreased PV but without an increase in RBCs
- dehydration, diuretic use, diarrhea etc
- corrected by increasing vascular fluid volume

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65
Q

absolute polycythemia

A

increase RBC mass

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66
Q

two types of absolute polycythemia

A

Primary: neoplastic (polycythemia vera)
- increase RBCs, WBCs and platelets
-causes blood hyperviscosity

Secondary : chronically increased [EPO]
- hypoxia related

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67
Q

Taylor has all the classic signs of anemia – fatigue, lack of concentration, and higher than normal resting and submaximal heart rate. She mentions one week ago she suffered a physical trauma and lost significant blood (although not enough to require a transfusion). You feel confident that her anemia is due to acute blood loss. What initial lab findings would confirm your suspicions?
a) Microcytic and hypochromic RBCs. Normal reticulocyte count. b) Normocytic and normochromic RBCs. Slightly higher than
normal reticulocyte count. c) Microcytic and hypochromic RBCs. Slightly higher than normal
reticulocyte count.
d) Normocytic and normochromic RBCs. Normal reticulocyte count

A

b) Normocytic and normochromic RBCs. Slightly higher than
normal reticulocyte count.

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68
Q

Fast forward one month and Taylor is still anemic. This time her doctor is concerned that she may be developing an iron-deficiency anemia. What lab findings would assist in this diagnosis
a) Microcytic and hypochromic RBCs. Normal reticulocyte count. b) Normocytic and normochromic RBCs. Slightly higher than
normal reticulocyte count. c) Microcytic and hypochromic RBCs. Slightly higher than normal
reticulocyte count.
d) Normocytic and normochromic RBCs. Normal reticulocyte count

A

c) Microcytic and hypochromic RBCs. Slightly higher than normal
reticulocyte count.

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69
Q

antigens AKA immunogens

A

foreign substances that elicit specific responses

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70
Q

antibodies AKA immunoglobulins

A

made in response to the antigen

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71
Q

humoral response

A

principle defence against EXTRACELLULAR microbes and toxins

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72
Q

cell-mediated immunity

A

mediated by specific T lymphocytes and defends against INTRACELLULAR microbes (viruses)

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73
Q

MHC (aka HLA) molecules

A

membrane bound proteins that display peptides for
recognition by T cells. Involved in self-recognition & cell-to-cell communication

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74
Q

MHC molecules two classes

A

Two classes, closely related:
– MHC-I – recognized by CD8+ cytotoxic T-cells
– MHC-II – recognized by CD4+ helper T-cells

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75
Q

IgG:

A

circulates in body fluids, binding antigens
(most abundant)

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76
Q

IgA

A

found in secretions on mucous
membranes; prevents antigens from entering
the body

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77
Q

IgM

A

circulates in body fluids; has five units to
pull antigens together into clumps

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78
Q

IgD

A

found on the surface of B cells; acts as an
antigen receptor

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79
Q

IgE

A

found on mast cells in tissues; starts
inflammation; involved in allergy

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80
Q

T-lymphocytes:

A

Activate other T & B cells
– Control intracellular viral infections
– Reject foreign tissue grafts
immunity”
– Involved in delayed hypersensitivity rxns
“all cell mediated immunity”

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81
Q

Helper T cell (CD4+)

A

– “Master regulator” of immune system
– Recognize MHC II-Ag complexes
– Can themselves differentiate into
subpopulations (eg. TH1, TH2) with varying functions

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82
Q

Cytotoxic T cell (CD8+)

A

Kill virally infected or cancer cells by
recognizing MHC I-Ag complexes

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83
Q

Regulatory T Cell

A

Seem to play a role in suppressing excessive
immune responses

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84
Q

Active immunity

A

acquired through immunization or
actually having a disease
– Slower but provides longer lasting immunity

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85
Q

Passive Immunity

A

– transfer of protective antibodies
against an Ag (eg. in utero or breast milk, antiserum)
– Rapid but only short term protection

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86
Q

what is the immunoglobulin(s) that cross the placenta

A

IgG is the only class of immunoglobulins to cross the placenta * Largest amount of IgG crosses the placenta during the last weeks of
pregnancy
– Premature infants may be deficient

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87
Q

what does aging do to the immune response

A

Aging associated with decreased cell mediated & humoral
immunity
– increase infection susceptibility
– increase autoimmune & immune complex disorders – increase incidence of cancer

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88
Q

Innate AKA natural or native

A

early, rapid response

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89
Q

Adaptive AKA specific or acquired

A

Develops later,
but more effective

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90
Q

Innate immunity

A
  • Always present, rapid
    response
  • Attacks non-self microbes * Does not distinguish
    between different microbes * Mechanisms include:
    – Epithelial barriers
    – Phagocytic leukocytes
    (eg. neutrophils &
    macrophages)
    – Specialized lymphocytes
    (eg. NK cells)
    – Plasma proteins (eg.
    complement)
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91
Q

Adaptive Immunity

A
  • Attacks specific microbes
    (antigens or Ag)
  • Longer response time,
    develops after exposure
    to specific Ag
  • Immunological “memory” * Mechanisms include:
    – Humoral immunity –>
    antibodies from B cells
    (blood & mucosal fluid)
    – Cell-mediated immunity
    –>T cells
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92
Q

True or false?
A vaccination is an example of adaptive immunity

A

True

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93
Q

where do B adn T cells mature?

A

B” cells mature in Bone marrow – “T” cells mature in the Thymus gland

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94
Q

chemokines

A

attract and activate WBCs

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95
Q

colony-stimulating factors

A

stimulate bone
marrow stem cells to divide and mature
– GM-CSF, G-CSF, M-CS

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96
Q

If an epithelial barrier is breached, the
early response cell is the

A

neutrophil

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97
Q

NK cells can directly

A

kill abnormal cells

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98
Q

opsonins

A
  • various soluble proteins that “tag” microorganisms
    for phagocyte recognition
  • Once the opsonin-coated microbe attaches to a
    complementary receptor on a phagocytic cell,
    phagocytosis is activated
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99
Q

inflammatory cytokines

A

– eg. TNF-α, IL-1, IL-6, IL-12,
interferons & chemokines
* Produces chemotaxis of leukocytes, stimulates acute-
phase protein production, inhibits viral replication

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100
Q

true or false
lipids are insoluble in plasma

A

true

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101
Q

5 types of lipoproteins

A
  1. chylomicrons
  2. VLDL
    3.IDL
    4.LDL
    5.HDL
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102
Q

what is Chylomicrons made out lof

A

80-90% triglycerides
2% protein

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103
Q

VLDL made of

A

55-65% triglycerides
10% cholesteral
5-10% protein

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104
Q

LDL made of

A

10% triglycerides
50% cholesterol
25% protein

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105
Q

HDL made of

A

5% triglycerides
20% cholesterol
50% protein

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106
Q

Apo(lipo)proteins:

A

– increase stability of LP
– Activate enzymes
involved in LP
metabolism
– Receptor recognition
in peripheral tissues

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106
Q

Apo(lipo)proteins exist in
two classes

A

– Exchangeable (eg.
apoA-I, apoC-II &
apoE)
– Nonexchangeable
(apoB-48, apoB-100)

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106
Q

exogenous intestinal pathway

A

– Involved in the transport
of dietary cholesterol & TGs from intestine to liver & other tissues (muscle, adipose tissue)
– In the form of
chylomicron

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107
Q

Endogenous hepatic pathway

A

– The processing of cholesterol & TGs by the liver and distribution to tissues
– In the form of VLDL, IDL

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108
Q

what are lipids absorbed from. the intestine as?

A

Dietary lipids are absorbed from intestine as chylomicrons (into lymphatic system & bloodstream)

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109
Q

Chylomicrons deliver what
(2)

A

(a) dietary cholesterol to the liver and (b) TGs to adipose tissue & muscle

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110
Q

what does the liver make and release

A

VLDL which delivers TGs to tissues

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111
Q

As VLDLs lose TGs, they become

A

IDLs

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112
Q

IDLs lose more TGs and become

A

LDLs

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113
Q

HDL carries ….

A

cholesterol from peripheral tissues back to liver (“reverse cholesterol transport”)

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114
Q

LDL

A

—low-density lipoproteins (“bad”)

– Lower density: decrease protein, increase cholesterol

– Transports cholesterol from the liver to tissues

– Can be oxidized and deposited on vessel walls
(triggers the atherosclerotic process)

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115
Q

HDL

A
  • HDL—high-density lipoproteins (“good”)

– Higher density: increase protein, decrease cholesterol

– Transports cholesterol from tissues to the liver

– Facilitates the clearance of cholesterol from atheromatous plaques and transports it to the liver, where it may be excreted

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116
Q

hyperlipidemia

A

increase of any/all lipids and/or LPs in blood

– Primary (inherited): genetic basis

– Secondary (acquired): due to diabetes, thyroid/renal/liver
disease, Cushing syndrome, obesity, alcoholism, drugs

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117
Q

Hypercholesterolemia

A

increase in cholesterol in blood
– Primary: eg. familial hypercholesterolemia (mutation in LDL
receptor gene)

– Secondary due mainly to lifestyle factors (eg. obesity,
diabetes, sedentary lifestyle)

  • High calorie diets increase production of VLDL –> increase LDL
  • Excess cholesterol ingestion may decrease LDL receptor
    synthesis, which decreases LDL removal from the blood
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118
Q

TC =

A

VLDL + LDL +
HDL

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119
Q

Statins

A

decrease or block the hepatic
synthesis of cholesterol thus
decrease LDL
* Also lower TG levels

120
Q

Which vessel layer can “expand” or “contract” to
accommodate or adjust pressure within the vessel?
A. Tunica intima
B. Tunica media
C. Tunica externa

A

tunica media

121
Q

skip

A
  • Monocytes attach to the endothelium –>
    macrophages
  • Macrophages release free radicals –>
    oxidizes LDL (endothelial toxin)
  • Macrophages ingest oxidized LDL –>
    become foam cells
  • WBCs, platelets, and vascular endothelium
    release chemicals that promote plaque
    formation
  • Plaques can block arteries or rupture &
    cause a thrombus
122
Q

atherosclerosis stage 1

A

Endothelial cell injury leading to adhesion of monocytes & platelets

123
Q

atherosclerosis stage 2

A

Migration of inflammatory cells into the intima
– Monocytes transform into macrophages that begin to engulf
LDL

124
Q

atherosclerosis stage 3

A

Lipid accumulation and smooth muscle cell proliferation
– Activated macrophages oxidize LDL (ROS release)
– Oxidized LDL is then aggressively ingested by macrophages
leading to foam cell formation – GFs also lead to proliferation of smooth muscle cells & increase ECM

125
Q

atherosclerosis stage 4

A

Plaque formation
– Formation of a fibrous cap (smooth muscle cells & dense ECM) with
a cellular “shoulder” & a necrotic “core” (lipid laden foam cells & fatty debris)
– Rupture of an unstable cap can lead to bleeding or thrombotic
vessel occlusion

126
Q

non- modifiable (atherosclerosis)

A

– Age, male gender, genetic disorders of lipid metabolism, family hx of premature CAD

127
Q

Potentially modifiable (atherosclerosis)

A

– Smoking, obesity, hypertension, hyperlipidemia with increase LDL & decrease HDL, diabetes

128
Q

no-traditional (atherosclerosis)

A

– Chronic inflammation eg. C-reactive protein (CRP)
–acute-phase protein for systemic inflammation
– increase lipoprotein (a) levels in blood (altered form of LDL that
contains apo-B-100)

129
Q

manifestations of atherosclerosis in the heart

A

Heart –> stable angina or acute coronary
syndrome = myocardial infarction or unstable angina

130
Q

manifestations of atherosclerosis in the aorta

A

aneurysm

131
Q

manifestations of atherosclerosis in the brian

A

transient ischemic attack or cerebrovascular accident

132
Q

manifestations of atherosclerosis in the legs

A

peripheral arterial disease

133
Q

manifestations of atherosclerosis in the bowel

A

bowel infarction

134
Q

What immediate threat do unstable plaques present
A. Clot formation will increase pressure in the vessel.
B. Plaque may lead to angina (chest pain).
C. Clots may break loose and block blood flow to key
organs.
D. All of the above constitute immediate threats

A

c

135
Q

“True” vs. “false” aneurysms

A

Unlike a true aneurysm, a pseudoaneurysm does not contain any layer of the vessel wall. Instead, there is blood containment by a wall developed with the products of the clotting cascade.

136
Q

what happens during SBP and DBP

A

SBP - ventricle contracts
DBP - ventricle relaxes

137
Q

pulse pressure =

A

SBP-DBP

138
Q

primary or essential hypertension

A

(no evidence of other diseases)
– ~90-95% of all cases (very common) – Genetics, ethnicity, age, diet, obesity, alcoholism

139
Q

secondary hypertension

A

(results from another disease/disorder)
– Renal hypertension, adrenocortical hormone
disorders, pheochromocytoma, aortic coarctation,
oral contraceptives

140
Q

target organ damage

A

is main concern (p.428)
– Kidneys, heart, eyes are particularly vulnerable but
all blood vessels may be affected
* Tx is lifestyle & pharmacologic:
– ACE inhibitors, diuretics, β-receptor inhibitors, Ca2+
channel blockers, etc

141
Q

orthostatic/postural hypotension

A
  • Abnormal drop in BP on
    assumption of standing
    position
  • Causes:
    – Reduced BV: diuretic use,
    vomiting, diarrhea
    – Drug induced hypotension
    (antihypertensives)
    – Aging – Bed rest & immobility (decrease PV)
    – ANS disorders
142
Q

deep venous thrombosis

A

Presence of thrombus in a vein and
the accompanying inflammatory response

143
Q

triad of thrombosis

A

– circulatory stasis + endothelial damage + hypercoagulability

144
Q

why do clots tend to form in leg veins

A

because they are deep large veins

145
Q

what are leg veins susceptible too?

A

blood
pooling and as venous return must
move against gravity, there is increase
chance of venous stasis

146
Q

what do leg veins have a risk of?

A

Risk of pulmonary embolism

147
Q

A patient takes a drug that is a sympathetic agonist. Which
of the following would you expect to occur
A. Increased heart rate and blood pressure
B. Increased heart rate and decreased blood pressure C. Decreased heart rate and increased blood pressure
D. Decreased heart rate and blood pressure

A

A

148
Q

what is the most common cause of coronary artery disease (CAD)?

A

atherosclerosis

149
Q

fixed atherosclerotic lesion

A
  • Associated with stable
    angina (if large enough
    to cause ischemia)
  • Have thick fibrous caps
  • Plaque usually partially
    obstructs vessels
  • Do not tend to form clots
    or emboli
150
Q

vulnerable atherosclerotic lesion

A
  • Associated with
    unstable angina & MIs * Have thin fibrous caps * Plaque can rupture &
    cause clot to form
    – May completely/
    incompletely occlude
    artery – May break free &
    become an embolus
151
Q

acute coronary syndrome

A

Ranges from unstable ischemia to acute MI (NSTEMI or
STEMI)

152
Q

ACS ECG changes can include

A
  • ECG changes can include:
    – T-wave inversion – ST-segment depression or elevation – Abnormal Q waves
153
Q

ACS serum cardiac markers

A
  • Serum cardiac markers (p.449)
    – Proteins released from dead/necrotic heart cells
    º Myoglobin, CK-MB, cardiac-specific TnI & TnT
154
Q

ACS Why are T waves and the ST segment first to be involved?
(ST parT)

A

– ST segment
* Is usually a flat, isoelectric line and represents the early start of ventricular
repolarization
* “Current of injury” created between normal cells and ischemic cells causing
deviation in normally flat ST segment –> elevated or depressed ST segment

155
Q

ACS Why are T waves and the ST segment first to be involved?
T PART

A
  • Is usually upright in Lead II & represents ventricular repolarization * Ischemic cells no longer normally repolarize –> often inverted in Lead 2
156
Q

ACS what about the abnormal Q waves

A

– Scar tissue due to a MI does not transmit electrical activity
– Ventricles may not depolarize normally leading to changes in Q waves

157
Q

signs and symptoms of acute myocardial infarction

A
  • Chest pain!
    – Severe, crushing, constrictive OR like heartburn
  • SNS response
    – GI distress, nausea, vomiting
    – Tachycardia and vasoconstriction
    – Anxiety, restlessness, feeling of “impending doom”
  • Hypotension and shock
    – Weakness in the arms and legs
158
Q

treatment of acute coronary syndromes

A

*O 2
* Drugs:
– Aspirin
– Nitrates
– Morphine
– Anticoagulants
– β-blockers
– ACE inhibitors * Reperfusion therapy
– Fibrinolytic drugs
– Stent insertion (PTCA)
– CABG surger

159
Q

myocardial infarction recovery 3 zones of tissue damage

A

– Necrotic zone (replaced with scar tissue)
– Surrounding injured/hypoxic cell zone
– Ischemic outer zone

160
Q

what is critical about Myocardial infarction recovery?

A

Timeliness of Tx is critical to re-establish blood flow &
limit damage! (20-40 mins)

161
Q

what are the problems with the scar tissue in myocardial infarction

A
  • Fibrous scar tissue lacks the contractile, elastic &
    conductive properties of normal myocytes
    – Complications are determined by extent/location of injury
162
Q

chronic ischemic heart disease

A
  • Imbalance in myocardial O
    2
    supply vs. demand due to:
    – decrease blood supply (due to atherosclerosis or vasospasm)
    –increase O2
    demand (due to stress, exercise or cold)
163
Q

3 classifications of chronic ischemic heart disease

A
  1. Chronic stable angina
  2. Silent myocardial
    ischemia (no pain)
  3. Variant (vasospastic or
    Prinzmetal) angina
164
Q

(CIHD) Stable angina

A

– fixed coronary obstruction that can occlude
blood flow
– Typical angina – Usually provoked by PA or stress and relieved by rest or nitroglycerin

165
Q

CIHD - variant angina

A

– coronary artery spasm. Etiology not known, but endothelial dysfunction, hyperactive SNS, etc. may contribute
– Angina that occurs at rest or during night

166
Q

CIHD - silent myocardial ischemia

A

– same causes as stable angina, but
anginal pain not experienced
– Ischemic episodes may be shorter and involve less myocardium – Defects in pain tolerance or pain transmission, or autonomic neuropathy
with sensory denervation

167
Q

valvular heart disease 2 types of mechanical disruption

A

stenosis and regurgitation

168
Q

stenosis

A

Valve will not open correctly
(valve narrowing)

– Harder to force blood through

– Will hear murmur of blood
shooting through the narrow
opening when the valve is open

169
Q

regurgitation

A

Valve will not close
correctly

– Leaks when “closed”

– Will hear a murmur of blood
leaking back through when the
valve should be closed

170
Q

valve disorder

A
  • Most commonly
    affect mitral & aortic
    valves
171
Q

If A/V valves leading
into the ventricles do
not work…?

A

mitral or tricuspid problems

172
Q

if semilunar valves leading out of the ventricles do not work…?

A

aortic or pulmonary problems

173
Q

mitral valve disorders

A

– Mitral valve stenosis
– Mitral valve
regurgitation – Mitral valve prolapse
(“floppy” valve)

174
Q

aortic valve disorders

A
  • aortic valve stenosis
  • aortic valve regurgitation
175
Q

cardiomyopathies

A

Disorders of heart muscle & myocardial performance
(mechanical or electrical in nature)

176
Q

primary cardiomyopathy

A

(confined to myocardium)

– Genetic: HCM and arrhythmogenic right ventricular
dysplasia – Mixed: dilated and restrictive – Acquired: myocarditis (usually viral); peripartum and
Takotsubo cardiomyopathy

177
Q

Secondary cardiomyopathy

A

(associated with other disease conditions) – Drugs, diabetes, alcoholism, muscular dystrophy,
autoimmune disorders & cancer treatment (radiation & drugs)

178
Q

hypertrophic cardiomyopathy

A

Unexplained left ventricular hypertrophy due to an autosomal dominant disorder

179
Q

hypertrophic cardiomyopathy more info

A

Contractile protein mutation –> weak myocytes
– Myocytes hypertrophy to compensate (esp. LV) – Paradoxical decrease in SV due to decrease diastolic filling
* Myocytes need more O2 and perform less efficiently
– Prone to heart failure and potentially SCD during exertion
– HCM is most common cause of SCD in young athletes

180
Q

what is hypertrophic cardiomyopathy most common cause of?

A

most common cause of sudden cardiac death in young athletes

181
Q

symptom of HCM

A

Dyspnea, chest pain & post
exertional syncope

182
Q

diagnosis and treatment of hypertrophic cardiomyopathy

A

Diagnosis by 2Decho + ECG

  • Tx: symptom management
    – β-blockers – Ca2+ channel blockers
183
Q

heart disease congenital disorder

A

– ~ 1 out of every 125 infants

– Weeks 3-8 after conception

– Contributing factors:

  • Genetic and chromosomal
  • Viruses
  • Drugs
  • Radiation
184
Q

heart disease acquired disorders

A
  • kawasaki disease
185
Q

true or false

Chronic ischemic heart disease is more likely to result in
stable angina than acute coronary syndromes

A

true

186
Q

true or false
Mitral valve regurgitation results in a diminished stroke
volume.

A

true - if the mitral valve doesnt close as it should, a portion of the stroke volume leaks back into the left atrium so it will decrease stroke volume

187
Q

heart failure

A

Complex syndrome resulting from functional or structural
impairment of ventricular filling or ejection

188
Q

heart failure can be caused by

A

– Pericardial disorders
– Myocardial disorders
– Endocardial disorders
– Valve problems
– Disorders of great vessels
– Metabolic abnormalities

189
Q

which populations have a high cardiac reserve and who has the lowest \?

A

athletes have a high one ~5-6x at rest

heart failure pationts may reach theirs at rest

190
Q

stroke volume equals

A

end diastolic volume - end systolic volume

191
Q

ejection fraction =

A

sv - edv (~60% at rest in healthy person)

192
Q

Q =

A

sv x hr

193
Q

pre-load

A

= volume of blood entering/stretching the ventricle

194
Q

frank starling mechanism

A

increase preload –> increase stroke volume

195
Q

afterload

A

force that ventricle must generate

196
Q

Systolic (HFrEF) or diastolic (HFpEF) failure

A

– Is the heart failing to pump? (EF <40%)
* Impaired contractility, valve problems or pressure issues
– or is it resisting filling from body/lungs? (EF >50%)
* Hypertension, constrictive pericarditis, HCM, aging, obesity , diabetes

197
Q

L-sided or R-sided failure

A

– If LV fails, blood backs up in the pulmonary circulation

  • Due to hypertension, acute MI (in LV) or valve problems

– If RV fails, blood backs up in the systemic circulation

  • Due to LV failure, pulmonary hypertension, valve problems, MI (in RV) or cardiomyopathy
198
Q

manifestations of heart failure

A
  • Fluid retention/edema
    – Due to increase capillary hydrostatic pressures * Respiratory mechanisms
  • Dyspnea
  • Orthopnea
  • Paroxysmal nocturnal dyspnea * Fatigue/exercise intolerance, weakness, cognitive impairment
    – Due to decrease Q
  • Cachexia & malnutrition
    – Tissue wasting due to decrease appetite & congestion of liver/GIT
  • Cyanosis
    – Due to decrease SaO2
  • Arrhythmias & SCD
    – AF & VF
199
Q

is edema consistent with left or right sided heart failure

A

r-sided

200
Q

edema

A

Capillary fluid moves into alveoli
– The lung becomes stiffer
– Harder to inhale (increase work of breathing)
– Edema –> decrease gas exchange in alveoli –> decrease Sao2
– Crackles
– Frothy pink sputum possible (due to the blood in the capillaries)

201
Q

treatment of heart failure

A

Lifestyle/counselling
– Individualized exercise training, Na+ & fluid restriction &
weight management

Pharmacological:
– Diuretics
* Promote loss of H2o & decrease volume overload (decreasing edema)
– ACE inhibitors
* Prevent angiotensin I –> angiotensin II
* Thus less vasoconstriction
* Also decrease aldosterone –> decrease Na+ & H2O retention
– β-adrenergic receptor blockers
* decrease SNS influence–> decrease workload of the heart –> decrease LV

202
Q

true or false
The characteristic pink sputum produced in pulmonary
edema is tinged with blood

A

true

203
Q

hypovolemic shock

A

Acute loss of
>15% BV,
causing
inadequate
filling of the
vascular
compartment
caused by:

– Whole blood
– Plasma
– ECF
– Dehydration
– Internal
bleeding

204
Q

cardiogenic shock

A

The heart fails to pump blood adequately
– eg. acute MI, valve disorders, arrhythmia, cardiomyopathy

205
Q

cardiogenic shock results in

A

– decrease Q –> decrease BP
– increased SNS response
– Peripheral vasoconstriction (but this increase TPR)
– Note increase workload on the heart can worsen heart failure
* Tx: treat underlying problem & decrease workload on heart

206
Q

manifestation and tx for hypovolemic

A

– Thirst, increase HR, cool/clammy skin, decrease BP, oliguria, neurologic
changes, etc.
– Tx: correct/control underlying cause & improve tissue
perfusion, O2
admin

207
Q

manifestations and tx for cardiogenic shock

A

– Consistent with end stage heart failure: cyanosis (lips, nail
beds, skin), decrease BP, decrease PP, oliguria, neurologic changes

– Tx: A delicate balance of increase Q, decrease myocardial O2 demand &
decrease myocardial blood flow
* Drugs which increase myocardial contractility w/o increasing HR (eg.
dopamine, dobutamine

208
Q

normovolemic shock

A

normal blood volume

209
Q

neurogenic shock

A

a condition in which you have trouble keeping your heart rate, blood pressure and temperature stable because of damage to your nervous system after a spinal cord injury

210
Q

septic shock

A

a life-threatening condition that happens when your blood pressure drops to a dangerously low level after an infection

211
Q

major complications of shock

A
  • Acute lung injury/respiratory distress syndrome
  • Acute renal failure
  • GIT complications
  • Disseminated intravascular coagulation
  • Multiple organ dysfunction syndrome
212
Q

Which type of shock is caused by low blood volume
A. Cardiogenic
B. Hypovolemic
C. Distributive
D. Septic

A

b. hypovolemic

213
Q

hypoxemia

A

low levels of oxygen in the blood

214
Q

HYPERCAPNIA

A

when you have too much carbon dioxide (CO2) in your blood

215
Q

true or false
Both hypercapnia and hypoxemia will lead to respiratory
failure if untreated.

A

true

216
Q

two types of bronchial asthma

A

atopic (extrinsic) asthma
non-atopic (intrinsic) asthma

217
Q

atopic (extrinsic) asthma

A

asthma triggered by allergens like pollen, pets, and dust mites.

218
Q

non atopic asthma

A

asthma that isn’t related to an allergy trigger like pollen or dust.

219
Q

chronic obstructive airway diseases

A

chronic bronchitis
emphysema
cystic fibrosis

220
Q

chronic bronchitis

A

overproduction and hypersecretion of mucus by goblet cells, which leads to worsening airflow obstruction by luminal obstruction of small airways, epithelial remodeling, and alteration of airway surface tension predisposing to collapse.

221
Q

asthma

A

a chronic inflammatory disease of the airways

commonly appears before age 5

222
Q

pathogenesis of asthma

A

Genetic predisposition (eg. Allergy or defects in bronchial endothelium)
✚
Environmental factors (ie. allergens, excessive hygiene, antibiotics from 0-2 yrs)
=
Predisposed to airway hyper-responsiveness

223
Q

atopic (extrinsic) asthma triggers

A

*Pet hair or dander
*Dust
*Chemicals in the air or in food
*Mold
*Pollen
*Tobacco smoke
*NOTE: Aspirin and NSAIDS can be trigger

224
Q

non atopic (intrinsic) asthma

A

*Respiratory infections
*Exercise
– (Warm ups are important!)
*Hyperventilation
*Cold air
*Inhaled irritants
*Aspirin and other NSAIDs

225
Q

1st exposure to allergen

A

Immune response stimulates B lymphocytes to
produce IgE which binds to mast cells =
sensitized mast cells

226
Q

2nd exposure to SAME allergen

A

– Early response: Allergen x-links with IgE’s on
mast cells = mast cells release histamine, leukotrienes, and inflammatory mediators

– Late response: Activated mast cells release
cytokines and cause WBCs like eosinophils to be
released = affect airways, eyes & nose

227
Q

atopic asthma

A
  • Type I hypersensitivity
    – ie. rapid & IgE mediated
  • Allergen
    –> Mast cells release inflammatory mediators
  • Cause acute early-response
    within 10-20 mins
    –> WBCs enter region and
    release more inflammatory
    mediators
  • Airway inflammation causes
    late-phase response in 4-8 h
228
Q

nonatopic asthma

A

Respiratory infections
– Epithelial damage, IgE production

  • Exercise, hyperventilation, cold air
    – Loss of heat and water may cause bronchospasm
  • Inhaled irritants
    – Inflammation, vagal reflex
  • Aspirin and other NSAIDs
    – Abnormal arachidonic acid metabolism
229
Q

mild to moderate signs of asthma

A
  • Cough with or without sputum production
  • SOB that gets worse with exercise or activity
  • Chest tightness
  • Wheezing
230
Q

severe signs and symptoms of asthma

A
  • Anxiety/apprehension
  • Severe SOB / no wheezing / inaudible breath sounds
  • increase use of accessory muscles
231
Q

diagnosis of asthma

A

– Careful history & physical exam
* Portable PEF meters can be useful – Spirometry (decrease FEV1.0/FVC

232
Q

treatment of asthma

A

– “Quick relief” bronchodilator (usually β2-agonist)
– “Longer term” medications (eg. inhaled
corticosteroids) to decrease airway inflammation
– Identify allergens and reduce exposure

233
Q

Which of the following occurs in asthma?
A. Airway inflammation
B. Bronchospasm
C. Decreased ability to clear mucous
D. All of the above

A

D

234
Q

chronic obstructive pulmonary disease

A
  • Group of disorders
    characterized by chronic &
    recurrent airflow obstruction
    in the airways
    – Usually progressive
235
Q

emphysema

A

Loss of lung elasticity,
abnormal enlargement of
air spaces & destruction of
lung tissue

236
Q

mechanisms of COPD

A
  • Inflammation and fibrosis of the bronchial wall
  • Hypertrophied mucous glands –> excess mucus
    – Obstructed airflow
  • Loss of alveolar tissue
    – decrease SA for gas exchange
  • Loss of elastic lung fibers
    – Airway collapse, obstructed exhalation, air trapping
237
Q

risk factors for COPD

A
  • Hx of cigarette smoking or significant lifetime exposure
    to secondhand smoke
    – 85-90% of COPD patients have a hx of smoking
  • Hx of airway infections
  • Hx of chronic asthma or bronchial hyper-responsiveness
  • Environmental/occupational exposures to dusts and
    chemicals
238
Q

emphysema more in depth

A

Neutrophils in the alveoli
secrete trypsin
– increase neutrophil # due to
inhaled irritants can
damage alveoli
*α1-antitrypsin inactivates the trypsin before it can damage the alveoli
– A genetic defect in α1-
antitrypsin synthesis leads
to alveolar damage

239
Q

chest wall in emphysema

A
  • Destruction of lung
    tissue & enlargement of
    air spaces leads to:
    – Loss of elasticity
    – Airways collapse
    during expiration
    – Trapped air – Lung hyperinflation
    (“barrel chest”)
    – increase TLC
    – Diaphragmatic
    fatigue and acute
    respiratory failure
240
Q

chronic bronchitis more in depth

A

– increase # of goblet cells (mucus secretion)
– Mucus hypersecretion (hypertrophy of submucosal glands
in trachea & bronchi)
– Inflammatory infiltration & fibrosis of bronchiolar wall

241
Q

how is chronic bronchitis diagnosed

A

Diagnosed by a chronic productive (sputum) cough for
>3 consecutive months in at least 2 consecutive years
* Common in middle-aged men

242
Q

pink puffers

A

(usually emphysema)
– Pink = lack of cyanosis
–increase VE to maintain oxygen levels
– Dyspnea; increased ventilatory effort
– Use of accessory muscles; pursed-lip (“puffer”) breathing

243
Q

blue bloaters

A

(usually bronchitis- increase in mucus
production)
– Cyanosis
– Fluid retention due to R sided heart failure (due to hypoxic
pulmonary vasoconstriction/hypertension) – Cannot increase respiration enough to maintain O2 levels

244
Q

diagnosis of COPD

A

-medical history
- spirometry
- chest xray

245
Q

treatment of COPD

A

– Depends on stage
– Smoking cessation
– Reduce risk of RTIs
– Meds (bronchodilators)
–O2 therapy

246
Q

in a COPD client, exhalation is…?

A

inefficient and o2 levels in the lungs decrease

247
Q

If blood goes through the lungs filled with stale air

A

– Blood will not pick up enough O2
(potentially leading
to hypoxemia)
– Blood might even pick up CO2 (potentially leading to
hypercapnia

248
Q

Which chronic obstructive pulmonary disease primarily
affects the alveoli?

A

emphysema

249
Q

pulmonary embolism etiology

A
  • Blood borne substance lodges in branch
    of pulmonary artery (eg. DVT)
    – Causes reflex bronchoconstriction,
    pulmonary hypertension & R heart strain
250
Q

manifestations of pulmonary embolism

A

– Asymptomatic to breathlessness to death
– Massive embolus leads to sudden
collapse, severe chest pain, shock & LOC

251
Q

diagnosis and treatment of pulmonary embolism

A

– Imaging, history, ECG
– Thrombolytic meds if life-threatening
– Anti-coagulants

252
Q

two types of pulmonary hypertension

A

primary and secondary

253
Q

primary pulmonary hypertension

A

(increase in pulmonary BP in absence of another condition)

º Rare & debilitating
º Blood vessel walls thicken and constrict; can lead to R heart failure, low CO, and death

254
Q

secondary pulmonary hypertension

A

(increase in pulmonary BP
associated with other
cardiopulmonary conditions)

º increase of pulmonary venous pressure
(mitral valve disorders)
º increase pulmonary blood flow
(congenital heart diseases)
º Pulmonary vascular obstruction
º Hypoxemia

255
Q

R-sided heart failure secondary to lung disease or
pulmonary hypertension

A

decrease lung ventilation leads to:
* Pulmonary vasoconstriction- increase workload on right
heart (RV)
* decrease oxygenation causes kidneys to release EPO –>
more RBCs made –> polycythemia (makes blood
more viscous) which increases workload on the heart

256
Q

what is metabolic syndrome also known as

A

AKA “insulin resistance syndrome” or “syndrome X”

257
Q

hyperglycemia

A

– Intra-abdominal (visceral) obesity
– increase blood triglyceride levels
– decrease HDL levels
– increase blood pressure
– Systemic inflammation

258
Q

what do pancreatic acini secrete

A

digestive juices into the duodenum

259
Q

alpha cells secreate

A

glucagon

260
Q

beta cells secreate

A

insulin and amylin

261
Q

delta cells secreate

A

somatostatin

262
Q

what is each islet of langerhans composed of?

A

alpha, beta and delta cells

263
Q

what increases insulin secretion?

A

increase in blood glucose

264
Q

Insulin increase glucose uptake, use & storage:

A

1) increase Glycogenesis
2) increase Lipogenesis (glucose –> fat)
3) increase Protein synthesis

265
Q

Insulin decrease

A

Insulin decrease :
1) decrease Glycogenolysis
2) decrease Lipolysis
3) decrease GNG (amino acids –> glucose)

266
Q

how many chains does insulin have and where is it released from?

A

2 chains and beta cells

267
Q

If someone lacks insulin, what happens to:
– Blood glucose levels?
– Blood amino acid levels?
– Blood pH?
– Intracellular fat levels?
– Intracellular protein levels?
– Cell growth?

A

– Blood glucose levels? INCREASE
– Blood amino acid levels? INCREASE
– Blood pH? DECREASE
– Intracellular fat levels? DECREASE
– Intracellular protein levels? DECREASE
– Cell growth? DECREASE

268
Q

decrease blood glucose –>?

A

decrease blood glucose –> increase glucagon secretion
– increase blood amino acids also stimulate secretion

269
Q

Amylin (islet amyloid polypeptide):

A

decrease glucose absorption in
the small intestine; decrease glucagon secretion
– Secreted by pancreatic β-cells
– Possible role in causing type 1 diabetes?

270
Q

Somatostatin:

A

decrease GI activity; decrease glucagon & insulin secretion
– Secreted by pancreatic δ-cells

271
Q

Gut derived hormones that increase insulin release (incretins)

A

GLP-1 & glucose dependent insulinotropic polypeptide

272
Q

“Counterregulatory” hormones (antagonistic to insulin)

A

– Epinephrine
– Growth hormone
– Glucocorticoids (mainly cortisol)

273
Q

diabetes mellitus

A

Group of metabolic diseases characterized by
hyperglycemia resulting from defects in insulin secretion,
insulin action, or both

274
Q

Chronic hyperglycemia:

A

Long term damage/failure to
eyes, kidneys, nerves, heart & blood vessels

275
Q
A
  1. T1: β-cell destruction –> absolute insulin deficiency
    – 1A autoimmune (genetic + env. cause) or 1B idiopathic
  2. T2: insulin resistance and/or relative insulin deficiency
  3. Other types:
    – Genetic defects in β-cell function or insulin action
    – Secondary to other diseases, drugs, or transplant
  4. Gestational diabetes mellitus (GDM
276
Q

pathogenesis of T2DM

A

Combination of genetic & lifestyle
factors?
– Esp. obesity & physical inactivity *
Insulin resistance leads to initial
hyperinsulinemia to keep blood glucose normal
* Relative insulin deficiency:
– Insulin resistance or inadequate
secretory response
* Absolute insulin deficiency:
– Destruction of the beta cells * Complex - pathogenesis not
completely understood

277
Q
  • Relative insulin deficiency:
A

– Insulin resistance or inadequate

278
Q

absolute insulin deficiency:

A

– Destruction of the beta cells

279
Q

T1 and T2 timeline

A

T1 sudden onset; T2 more insidious

280
Q

the 3 polys

A

polyuria, polydipsia, polyphagia

281
Q

polyuria

A

your body makes more pee than normal

282
Q
A
283
Q

polydipsia

A

excessive thirst

284
Q

polyphagia

A

an abnormally strong, incessant sensation of hunger or desire to eat often leading to overeating

285
Q

management for both type of DM

A

Diet (both)

  • Exercise (both)
    – Note increase risk of hypoglycemia
  • Oral medications (T2), eg:
    – Metformin (biguanide) – Liraglutide (GLP-1 R agonist)
  • Insulin injections (T1 or T2)
    – Short, intermediate and long acting types
    – MDIs & CSII (insulin pump)
286
Q

oral medications of T2 DM

A

eg:
– Metformin (biguanide)

– Liraglutide (GLP-1 R agonist)

287
Q

Diabetic ketoacidosis

A

– Hyperglycemia + ketosis +
metabolic acidosis

– Reflects an insulin
deficiency (ie. more
common in T1)

288
Q

hypoglycemia

A

excess insulin or insufficient food

289
Q

Hyperglycemic hyperosmolar
state

A

–H2O is pulled out of body cells, incl. brain

290
Q

How would hyperglycemia with ketoacidosis cause:
– Heavy breathing?
– Fruity smelling breath?
– Polyuria?
– Thirst?
– Dehydration?

A

– Heavy breathing? because of metabolic acidosis
– Fruity smelling breath? keto acids
– Polyuria? osmotic diuresis
– Thirst? water is moving out of cells
– Dehydration? polyuria and osmotic diuresis

291
Q

DM chronic complications

A

Somatic:
* Sensory –> decrease perception &
hypersensitivity issues

  • Motor –> balance deficits
    – Autonomic (defects in vasomotor,
    cardiac responses, bladder problems,
    GIT problems, erectile problems)
292
Q

nephropathies

A

renal failure

293
Q

retinopathies

A

blindness

294
Q

other chronic complications for DM

A

Macrovascular complications
– increase atherosclerosis, CAD, CVD & PVD
* Foot ulcers due to neuropathy
* Infections

295
Q

Which of the following is a complication of diabetes
mellitus?
A. Nephropathy
B. Retinopathy
C. Neuropathy
D. All of the above

A

D. all of the above

296
Q

repair/regeneration of muscle occurs due to the presense of?

A

muscle satellite cells

297
Q

ossification

A

conversion of fibrocartilaginous cartilage to bone

298
Q

rheumatoid factor

A

antibody against IgG fragments in most patients

299
Q
A

AET 310 (1 decks)

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