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PMP 101 Health, Disease and Patient > Cardiovascular System II > Flashcards

Cardiovascular System II Flashcards

1
Q

Rediculocytes

A
  • Maturation ito red blood cells 3 day life span
  • then RBC survives for 120days
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2
Q

Regulation of erythropoiesis

A
  • Negative feedback the kidney becomes hyptoxic (O2 drops in renal artery)
  • Stimulated release of erythropoetin (EPO) then stimulates bone marrow to produce erythrocytes
  • New potential to carry oxygen by red blood cells
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3
Q

What is Hypoxia

A
  • Haemorrage or injury
  • iron deficincy
  • High altitude or lung disease
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4
Q

How do males have more blood Red blood cells than females?

A
  • Higher Testesterone enhances EPO production
  • High EPO therefore Erythrocytes mature faster
  • Increase haematocrit, dehydration and blood viscosity
  • Able to transport more oxygen for respiration
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5
Q

Importance of Iron in blood

A
  • 65% in Hb
  • Bound with protein and stored as ferritin and haemosiderin
  • Transported by binding with transferrin
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6
Q

How does Heam degrade?

A

Degraded to bilirubin, yellow pigment-Liver secretes bilirubin in bile (in intestine)-urobilinogen-stercoblin, brown pigment excreted in faeces

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7
Q

How does the globin degrade?

A

metabolised into aminoacids & recycled

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8
Q

Anaemia symptoms

A
  • Fatigue
  • Pallor
  • Dyspnoea & chills
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9
Q

Haemorrhagic

A
  • Acute or Chronic blood loss
  • Treatment blood transfusion
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10
Q

Iron deficiency

A

RBC turning microcytes lacking Iron-Hb production. Treat or manage with Iron supplements

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11
Q

Renal treatment

A

lack of EPO supplement with synthetic EPO

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12
Q

Pernicious

A
  • Autoimmune condition-destroy B12 absorption; without B12 RBC cannot divide or become macrocytes
  • Dietry supplement of B12
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13
Q

Aplastic

A

Injury to Red Bone Marrow/ Drugs: Chemotherapy, Radiation, chemicals

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14
Q

Thalassemia

A
  • Globin chain in Hb is absent or malfunction
    -RBC become thin, delicate and lack Hb
    -Mild to Severe subtypes- Blood transfusions
    -Predominantly in Mediterranean ethnics
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15
Q

Sickle cell anaemia

A
  • Mutation in Hb: one amino acid is wrong in the globin B chain (6th AA- Glutamic acid in normal RBC whereas 6th AA is Valine in sickle RBC)
  • Creasent shaped :
  • O2 levels are lower
  • Crescent shape block flow in the blood vessels and leads to stroke and other vascular diseases
  • predominently in African ethnics
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16
Q

Polycythaemia (too many RBC)

A
  • Too thick too many cells increase the viscosity
  • Stroke
    -Coronary artery disease
    -Renal disease
17
Q

Stages of Haemostasis

A

1) Vascular spasm
2) Platelet Activation- Plug
3) Coagulation- Patch

18
Q

Haemostasis

Vascular Spasm

A
  • Pain reflux so constriction of vascular smooth muscle
  • Trigger clotting chemicals/factors needed & directed to site of injury
19
Q

Haemostasis

Platelet Activation- Plug

A
  • Endothelial Damage so Collagen exposed
  • Platelets stick to exposed collagen is activated
  • Platelets stimulate ADP, Thromboxane A2 and Serotonin
  • Von Willebrand Factor- Stabilise collagen-platelet adhesion
  • Positive feedback - more platelet release
20
Q

Haemostasis

Coagulation- Patch

A
  • Clotting factors (procoagulants) in Liver
    Vitamin K, the biosynthesis clotting factors
    Plasma proteins I to XIII
  • Happens while platelet activation occours
21
Q

X-A prothromin Activator

A
  • Intrinsic (blood) and extrinsic activates (tissue level) to x Prothrombin
  • Converted into Thrombin (can go straight to fibrin mesh
  • Fibrinogen (soluble)
  • Fibrin (insoluable)
  • Fibrin mesh

i

22
Q

Clot retraction countercurrent with vessel

A
  • Actin and myosin in platelet contracts pulls fibrin
  • Platelet-derived growth factor which stimulates smooth muscle
  • Vascular endothelial rebuilds endothelial lining by multiplying endothelial cells
23
Q

Fibrinolysis

A

Plasma protein trapped in clot- converted Plasmin-digest Fibrin

24
Q

Thrombosis

A

Blood clotting (Thrombus) in arteries, veins or capillaries

25
Q

Embolism

A

Blood clot/endogenous materials (Embolus) moving in the blood vessel and obstructing blood flow

26
Q

Liver dysfunction

A

Clotting factors synthesis
Malnutrition of Vitamin
Hepatitis, Cirrhosis
Impaired Bile production- needed for fat and vit.K absorption

27
Q

A blood group

A
  • Antigen A on red blood cell
  • Antibody B attaches immunoglobin
28
Q

B blood group

A
  • Antigen B on red blood cell
  • Antibody A attaches immunoglobin
29
Q

AB blood group

A
  • Antigen A and B
  • There are no antibodies
30
Q

O group

A
  • No antigens on red blood cell
  • Has both A and B antibodies
31
Q

Rhesus factor

A
  • Carry Rhesus factor which is antigen D so will be positive

PMP 101 Health, Disease and Patient (64 decks)

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